Postoperative infectious complications in surgery. What you need to know about anaerobic infection? Features of bacteriological research in anaerobic infection

Symptoms depend on the location of the infection. Anaerobes are often accompanied by the presence of aerobic organisms. Diagnosis is clinical, along with Gram stain and cultures for 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, oral cavity, gastrointestinal tract, and vagina. If these ratios are disrupted (eg, by surgery, other trauma, impaired blood supply, or tissue necrosis), some of these species can cause infections with high morbidity and mortality. Once implanted in the main site, the organisms can hematogenously reach distant sites. Because aerobic and anaerobic bacteria are often present in the same infected site, appropriate screening and culture procedures are needed to avoid screening anaerobes. Anaerobes can be a major cause of infection in the pleural cavities and lungs; in the intra-abdominal, gynecological, central nervous system, upper respiratory tract and skin diseases, and in bacteremia.

Causes of anaerobic infections

Major anaerobic Gram-negative bacilli include Bacteroides fragilis, Prevotella melaninogenica and Fusobacterium spp.

The pathogenesis of anaerobic infections

Anaerobic infections can usually be characterized as follows:

• They tend to appear as localized collections of pus (abscesses and cellulitis).
• O2 reduction and low oxidation reduction potential, which predominate in avascular and necrotic tissues, are critical to their survival,
• In the case of bacteremia, it usually does not lead to disseminated intravascular coagulation (DIC).

Some anaerobic bacteria have overt virulence factors. The virulence factors of B. fragilis are probably somewhat exaggerated due to their frequent occurrence in clinical specimens, despite their relative rarity in the normal flora. This organism has a polysaccharide capsule, which obviously stimulates the formation of a purulent focus. An experimental model of intra-abdominal sepsis has shown 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, is involved in septic shock associated with Fusobacterium severe 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 intra-abdominal sepsis and mixed anaerobic pneumonias is high. B. fragilis bacteremia has a high mortality rate, especially among the elderly and cancer patients.

Symptoms and signs of anaerobic infections

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

For certain 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.
• Bad smell 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 taken from normally sterile areas are used for culture because other organisms present can easily be mistaken for pathogens.

Gram stain and aerobic cultures should be obtained for all samples. Gram stains, especially in the case of bacteroid infection, and cultures for all anaerobes may be false 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 sensitivity pattern can usually be predicted. Therefore, many laboratories do not routinely test anaerobic organisms for susceptibility.

Treatment of anaerobic infections

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

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

Since the results of studies on anaerobic flora may not be available within 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 penicillin-allergic patients, clindamycin or metronidazole (plus a drug active against aerobes) is good.

Gastrointestinal tract infections or female pelvic anaerobic infections are likely to necessarily 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 varieties. The resistance of B. fragilis and other obligatory gram-negative bacilli to penicillin and cephalosporins of the 3rd and 4th generations differs. However, the following drugs have excellent activity against B. fragilis and efficacy in vitro: metronidazole, carbapenems (eg, imipenem/cilastatin, meropenem, ertapenem), inhibitor combination, tigecycline, and moxiflocacin. No single drug can be given preference. Drugs that appear to be somewhat less active against B. fragilis in vitro are usually 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 a unique anaerobic bactericidal capacity, and is not commonly prescribed due to pseudomembranous colitis sometimes associated with clindamycin. Concerns about the potential mutagenicity of metronidazole have not been clinically supported.

Since 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 enteric Gram-negative bacilli) and an antibiotic active against B. fragilis is no longer advocated.

Prevention of anaerobic infections

• Metronidazole plus gentamicin or ciprofloxacin.

Before elective colorectal surgery, patients must be prepared for the procedure, the intestines, 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. Oral examples 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 purulent complications, and prevent spread of infection around the surgical site.

For patients with a confirmed allergy or adverse reaction to β-lactams, the following are recommended: clindamycin plus gentamicin, aztreonam, or ciprofloxacin; or metronidazole plus gentamicin or ciprofloxacin.

Prevention of tetanus. Emergency prophylaxis of tetanus involves not only the primary surgical treatment of the wound with the removal of foreign bodies and necrotic tissues, but also the creation (if necessary) of specific immunity against tetanus.

Emergency specific prevention of tetanus is carried out for: injuries with violation of the integrity of the skin and mucous membranes, frostbite and burns of the second, third and fourth degree, community-acquired abortions and childbirth, gangrene and tissue necrosis, with long-term abscesses and carbuncles, penetrating wounds of the gastrointestinal tract, animal bites.

Drugs used for emergency immunoprophylaxis of tetanus:

Adsorbed tetanus toxoid (AS-toxoid) is a vaccine for the prevention of tetanus, intended primarily for emergency immunization.

Vaccination regimen: a full course of vaccinations consists of two vaccinations of 0.5 ml with an interval of 30-40 days and revaccination after 6-12 months with the same dose.

Contraindications: first half of pregnancy.

Antigen-reduced adsorbed diphtheria-tetanus toxoid (ADS-M toxoid) is an antigen-reduced vaccine for the prevention of diphtheria and tetanus. Designed for immunization of children from 6 years of age, adolescents and adults.

Contraindications: There are no permanent contraindications.

Relative: after acute diseases, they are vaccinated 2-4 weeks after recovery, patients with chronic diseases are vaccinated upon reaching a complete or partial remission, people with neurological diseases are vaccinated after exclusion of the progression of the process, patients with allergic diseases are vaccinated 2-4 weeks after the end of the exacerbation.

Anti-tetanus horse serum, purified concentrated liquid (PSS) - contains antitoxins that neutralize tetanus toxin. Used for the treatment and emergency specific prophylaxis of tetanus

Composition: contains specific immunoglobulins - a protein fraction of the blood serum of horses hyperimmunized with tetanus toxoid or toxin.

Contraindications for use: the presence of hypersensitivity to the corresponding drug, pregnancy.

Adverse reactions: serum sickness, anaphylactic shock.

Due to the allergenicity of drugs, each vaccinated person must be under medical observation within an hour after vaccination. When symptoms of shock appear, urgent anti-shock therapy is necessary. Persons receiving PSS should be warned to seek immediate medical attention in case of fever, itching and skin rashes, joint pain, and other symptoms characteristic of serum sickness.

Tetanus toxoid human immunoglobulin (PSHI) is an immunologically active protein fraction isolated from the blood serum (plasma) of donors immunized with tetanus toxoid, purified and concentrated by fractionation with ethyl alcohol at a temperature below 0°C. Intended for emergency prophylaxis of tetanus instead of equine anti-tetanus serum in individuals who are particularly sensitive to equine protein.

Mode of application: the drug is administered once intramuscularly.

Contraindications: and immunoglobulin should not be administered to persons with a history of severe allergic reactions to the administration of human blood products.

The introduction of the above drugs is not carried out:

children and adolescents who have documentary evidence of scheduled preventive vaccinations in accordance with age, regardless of the period that has elapsed since the next vaccination;

children and adolescents who have documented evidence of a course of routine preventive vaccinations without the last age-related revaccination;

adults who have documented evidence of a full course of immunization not more than 5 years ago;

persons who, according to the data of emergency immunological control, have a titer of tetanus toxoid in the blood serum above 1:160 according to RPHA;

persons of all ages who received two vaccinations no more than 5 years ago, or one vaccination no more than 2 years ago;

children from 5 months of age, adolescents, military servicemen and those who have served in the army for a fixed period, whose vaccination history is not known, and there were no contraindications to vaccination;

persons who, according to the data of emergency immunological control, have a tetanus toxoid titer within 1:20, 1:80 according to RPHA (determination of tetanus immunity (PSI) is carried out in cases where there is no documentary evidence of immunization courses in a patient).

A full course of AS immunization for adults consists of two vaccinations with an interval of 30-40 days and revaccination after 6-12 months. In the abbreviated scheme, the full course of immunization includes a single dose of AC in a double dose and revaccination after 6-12 months.

Active - passive prophylaxis of tetanus (in this case, 1 ml of AS is administered, then - PSCI (250 IU) or after an intradermal test - PSS (3000 IU)) is carried out:

persons of all ages who received two vaccinations more than 5 years ago or one vaccination more than 2 years ago;

unvaccinated persons, as well as persons who do not have documentary evidence of vaccination;

persons who, according to the data of emergency immunological control, have a titer of tetanus toxoid less than 1:20 according to RPHA.

It must be remembered that all persons who received active-passive tetanus prophylaxis should be revaccinated with 0.5 ml of AS or 0.5 of ADS-M to complete the course of immunization in the period from 6 months to 2 years.

Prevention of anaerobic infection. Antigangrenous serum is used to prevent clostridial anaerobic infection.

Composition and form of release: 1 ampoule of a polyvalent drug with a prophylactic dose contains 10,000 antitoxins against three types of pathogens of gas gangrene (cl. perfringens, cl. novii, cl. septicum). The kit contains 1 ampoule of anti-gangrenous serum and 1 ampoule of serum diluted 1:100 for determining sensitivity to horse protein.

Indications: gas gangrene (treatment and prevention), gangrenous diseases: postpartum anaerobic sepsis, lung gangrene, etc.

Dosage and administration:

for prophylactic purposes - with a negative intradermal test, undiluted anti-gangrenous serum is injected subcutaneously in an amount of 0.1 ml and the reaction is observed for 30 minutes. If there is no reaction, the entire dose of serum is slowly injected intramuscularly.

for therapeutic purposes - 150,000 IU are administered intravenously, drip, diluting it 5 times with isotonic sodium chloride solution. Before the introduction of serum, an intradermal test is performed to detect sensitivity to horse protein: 0.1 ml of diluted 1:100 serum (located in a separate 1 ml ampoule) is intradermally injected into the flexor surface of the forearm and the reaction is observed for 20 minutes. The test is considered negative if the diameter of the papule is not more than 0.9 cm with a slight limited reddening of the skin around the papule.

The classic causative agents of gas gangrene are Cl. perfringens, Cl. oedematiens, Cl. hystolyticum, Cl. septicum, Cl. falax, Cl. sporogenes.

All of them secrete active exotoxins that cause necrosis of fatty tissue, connective tissue and muscles, hemolysis, vascular thrombosis, damage to the myocardium, liver, kidneys, and nervous tissue. The main components of exotoxin include: lecithinase C (necrotizing and hemolytic action), hemolysin (necrotizing and specific cardiotoxic action, which predetermines a lethal outcome), collagenase (a lethal factor due to lysis of protein structures), hyaluronidase (a factor of penetration, spread of infection), fibrinolysin ( lyses fibrin, predetermines DIC), neuraminidase (destroys immune receptors on red blood cells), hemagglutinin (inhibits phagocytosis), etc.

One of the main etiological features of anaerobic clostridial infection (ACI) is the polymicrobial association of anaerobes. All clostridia are characterized by gas formation and the development of edema in the tissues. Although in each case a certain microbe is predominant and leaves an imprint on the course of the disease. Cl. perfringens, which are more common, cause mainly the formation of a large amount of gas in the wound, Cl. oedematiens - edema, Cl. septicum - edema and tissue necrosis. In addition, pathogens of gas infection can form associations with aerobic flora - staphylococcus, Proteus, intestinal Escherichia, etc. Clostridial infection is characterized by extreme severity of the course, extensive necrotic changes, gas formation and high mortality from 27 to 90%.

However, the share of Clostridia among all pathogenic anaerobes does not exceed 4-5%. There is a much more numerous and significant group of anaerobes pathogenic for humans that do not form spores - non-spore-forming, non-clostridial. Many of them have a capsule, so they are resistant to drying out. The diseases they cause are called anaerobic non-clostridial infections (ANIs). Non-spore anaerobes, as a rule, are representatives of the normal human autoflora, living on the surface of the skin, in the respiratory tract and, especially, in the lumen of the gastrointestinal tract, that is, they are of endogenous origin. ANI is not uncommon, often does not have clinical uniqueness, and is constantly encountered in everyday surgical practice. But only in recent years has it become possible to reliably diagnose non-clostridial infections, thanks to the development of methods for bacterioscopic, bacteriological and physicochemical identification of anaerobic microorganisms. They play an extremely important role in the development of acute purulent diseases. It has been established that the frequency of isolation of anaerobes ranges from 40 to 95%, depending on the nature and localization of the inflammatory process.

Non-clostridial anaerobic pathogens include:

gram-positive bacteria: Bifidobacterium, Eubacterium, Actinomyces, Arachiie, Lactobacillus;

gram-negative bacteria: various species of Bacteroides, Fusobacterium, Campylobacter:

gram-positive cocci: Peptococcus, Peptostreptococcus, Ruminococcuss;

Gram-negative cocci: Vielonella.

Gram-negative bacteria (Bacteroids, Fusobacteria) and Gram-positive cocci (Peptococcus and Peptostreptococcus) are of the greatest importance in the development of purulent-inflammatory diseases of soft tissues. With ANI, as well as with gas infection, a feature is the polymicrobial nature of the lesion with the participation in the association of 1-4 types of anaerobes and 2-5 types of aerobic flora (enterococci, -hemolytic streptococcus, staphylococci, enterobacteria, etc.). The synergism of anaerobes and aerobes has been known for a long time. On the one hand, aerobes absorb free oxygen in tissues, on the other hand, they secrete specific enzymes - catalase and superoxide dismutase, which protect anaerobes from oxygen exposure. These mechanisms are of greatest importance for API, since many non-spore pathogens are microaerophiles.

It should be emphasized that the division of anaerobes into AKI and API is very conditional, since they are fundamentally one group of infections, consisting of different nosological forms.

Clinically, anaerobic infection of soft tissues usually manifests itself in the form of phlegmon, the severity of which depends on the volume of affected tissues and the rate of progression and spread of inflammation. The infection can be localized mainly in the subcutaneous adipose tissue, in the fascia, in the muscles, or simultaneously affect these anatomical formations. The inflammatory process tends to spread through the interfascial spaces far beyond the primary focus of infection. The defeat of soft tissues is often complicated by thrombophlebitis of superficial and deep veins. Therefore, when examining patients, one should also pay attention to pain, soreness and swelling outside the primary lesion.

The incubation period for anaerobic infections ranges from several hours to 7 days. The clinical picture is determined by general and local manifestations. An anaerobic infection is characterized by an unusually strong burning pain in the primary focus (injection site, wound, etc.), severe intoxication, an increase in body temperature to 39 or more, tachycardia, a change in the patient's psyche - euphoria, excitement, replaced by pessimism, depression, lethargy. In laboratory studies, there is an increase in the number of leukocytes from 12-2010 9 /l to 26.110 9 /l; shift of the leukocyte formula to the left; an increase in the leukocyte index of intoxication (LII) from 3-7 to 21.4 arb. units; index of intoxication (GPI) from 3-7 to 50.6 arb. units (at a rate of 1.3-1.6 conventional units); indicator of molecules of average mass (MSM) more than 0.6-1.0 arb. units at a rate of 0.24 arb. units; a decrease in the distribution index (DI) of MSM from 1.2 to 0.73 (at a rate of 1.4). Quite characteristic is the development of early toxic anemia with a decrease in hemoglobin from 110-100 to 40-50 g/l; erythrocytes from 4.0-3.5 to 1.5-2.510 12 /l.

Rapidly progressive intoxication quickly leads to the development of systemic insufficiency, primarily cardiovascular, respiratory, hepatic, renal, endocrine, immune, in especially severe cases - to multiple organ failure. Inevitably, energy metabolism, acid-base, water-electrolyte and protein balance were disturbed, hormonal insufficiency developed, serious imbalances appeared in the coagulation and anti-coagulation system with the development of DIC. In the treatment of patients with anaerobic lesions, surgeons often encounter coma and collaptoid conditions against the background of intensive complex therapy, the genesis of which can be extremely difficult to establish without sufficient laboratory support (hypo- and hyperglycemia, hypokalemia, disorders of the ASC, vascular and heart failure, uremia, etc.). d.). To avoid this, it is necessary to actively monitor biochemical parameters, ECG, and central venous pressure. In the severe toxemia phase, this control should be carried out in the monitoring mode.

In the earliest stages of the disease, there is a discrepancy between the severity of toxemia and the scarcity of local manifestations. Meanwhile, local manifestations have a number of features characteristic of anaerobic damage. Knowing them is extremely important for the clinician, since the final identification of an anaerobic pathogen takes 5–8 days in a specialized medical institution, and a successful outcome can be expected only with immediately initiated complex treatment. The diagnosis of this pathology in a wide medical network should be based on clinical specific manifestations of anaerobic infection, due to the ecology of pathogens, their metabolism and pathogenicity factors.

In the circumference of the wound or injection, there is always a pronounced edema that does not leave a mark after pressing with a finger. Tissue edema is confirmed by clearly defined indentations at the hair root and the symptom of "cutting" the ligature.

In the affected area, patients note a very strong burning or arching pain, which is not relieved by analgesics and tends to increase over time. With a banal aerobic flora, the pain is moderate.

The skin in the area of ​​inflammation is tense, the color is often pale, shiny. Much less often, the skin against the background of edema is hyperemic without clear boundaries with a tendency to spread rapidly in all directions. With the involvement of the fascia in the inflammatory process and the development of thrombosis of small vessels (usually veins), areas of darkening or necrosis may appear on the skin, subepidermal dark cherry blisters may form.

The palpable presence of gas in the subcutaneous tissue (subcutaneous crepitus), in the intermuscular spaces, or in muscle sheath formations (movement of gas on deep palpation) often confirms the diagnosis. Gas in the tissues accumulates from the fact that during anaerobic metabolism, hydrogen, nitrogen and methane, which are poorly soluble in water, are released. Somewhat earlier and more reliably, gas formation can be detected radiographically (air bubbles in soft tissues) and ultrasound. The clinical, radiological and ultrasound examination in dynamics looks justified. At even earlier stages, one can see clinically small gas bubbles in the exudate during drainage of abscesses or at the time of opening and excising tissues. Naturally, the phenomenon of gas formation in tissues can be unequivocally taken into account in the absence of signs of its direct entry into tissues during trauma, especially the chest and hollow organs of the gastrointestinal tract. From a diagnostic point of view, gas formation in tissues is a very indicative symptom, but rare. It is more characteristic of anaerobic clostridial infection with a predominance of Cl in the microbial landscape. perfringens. In practice, at present, forms of anaerobic non-clostridial infection predominate, in which gas formation is scarce or absent altogether. In this regard, it should be especially noted that the established idea that anaerobic infection is necessarily accompanied by the formation of gas in the tissues is incorrect and outdated. In anticipation of its appearance, you can lose the patient. In these cases, attention should be paid to other clinical signs of anaerobic inflammation. Among our patients, the classical accumulation of gas in soft tissues with palpation of a "snow crunch", the presence of clear foci of darkening in the tissue, in the intermuscular sections, along the wound channel on x-rays, and its noisy release at the time of dissection of the muscle fascia was present in only one patient with a gunshot wound. hips. In all other patients, gas was detected during tissue excision or was absent altogether.

A rather constant symptom indicating the presence of anaerobes in tissues is an unpleasant putrefactive odor of exudate. The previously attributed property to give a similar smell to Escherichia coli turned out to be erroneous. Cultivation of isolated anaerobes in anaerobics with absolute constancy confirmed their involvement in the formation of unpleasantly smelling volatile sulfur compounds: hydrogen sulfide, methyl mercaptan and dimethyl sulfide.

A characteristic sign of anaerobic inflammation is the putrefactive nature of tissue damage. In the foci of infection, dead tissue is often found in the form of unstructured grey-dirty or gray-green detritus, sometimes with black or brown areas. They do not have clear boundaries and definite forms. Putrefactive damage to tissues is explained by the peculiarities of the metabolism of anaerobes - one of the elements of putrefaction is the process of anaerobic oxidation of the protein substrate.

The color and nature of the exudate has quite definite features. It is sparse, grey-green or brown in color. Coloring may be uneven. The exudate is usually very liquid, in the cellular layers it can be abundant, but for muscle infections, poor diffuse impregnation of tissues is more characteristic. Over time, with the addition of aerobic flora, the discharge from the wound may become mixed, and then purulent - a thicker consistency, dark yellow, homogeneous, odorless. It should be emphasized that the distinctive signs of exudate are most clearly detected in the early stages of the disease. The detection at the time of opening or revision of the wound of a combined lesion of the skin, subcutaneous tissue, fascia and muscles in the form of melting and gray-dirty or brown impregnation with a pungent odor clearly indicates an anaerobic lesion.

Most anaerobic infections are endogenous, ie. caused by the patient's own microflora. This implies their clinical feature - proximity to the natural habitats of anaerobes - the digestive tract, respiratory tract, hollow organs. Practice shows that anaerobic and mixed lesions often occur with injuries of the gastrointestinal tract with damage to the mucosa, with wounds and scratches in the perineum, with injections in the buttocks, with animal and human bites, as well as on the hands after blows to the teeth.

Anaerobic infections should be suspected when no pathogen can be isolated by the usual culture method, or when the number of isolated bacteria does not match what is seen in smears under a microscope, and also if the patient has 2-4 or more of the described local symptoms.

anaerobic infection

The classification of all microorganisms in clinical microbiology is based on their relationship to atmospheric oxygen and carbon dioxide. Using this principle, bacteria are divided into 6 groups: obligate aerobes, microaerophilic aerobes, facultative anaerobes, aerotolerant anaerobes, microaerotolerant anaerobes, obligate anaerobes. Obligate anaerobes die in the presence of free oxygen in the environment, facultative anaerobes are able to exist and develop both in the absence of oxygen and in the presence of it in the environment.

Anaerobes are called microorganisms that can exist and multiply in the absence of free oxygen in the environment; oxygen is not needed for their vital activity and reproduction.

All known anaerobic microorganisms can very often become the causative agents of a number of diseases. Among them are appendicitis, peritonitis, abscesses of various localization, pneumonia, pleural empyema, etc. Among the diseases caused by anaerobic microflora, tetanus and gas gangrene are the most severe.

Tetanus

Tetanus (tetanus) is a wound infectious disease caused by the toxin of the anaerobic spore-bearing bacillus Clostridium tetani when it enters the body through a defect in the skin or mucous membrane, characterized by damage to the nervous system, attacks of tonic and tetanic convulsions.

History: the oldest description of tetanus is found in a papyrus extracted from the pyramid of Cheops (2600 BC). In the works of Hippocrates, Galer, Pirogov, Galen, one can also find a description of the disease, which is embedded in the current concept of the disease as tetanus.

N.D. Monastyrsky (1883) discovered tetanus bacillus for the first time during microscopy. In 1890, Bering managed to obtain anti-tetanus serum.

Geographic distribution

Since ancient times, a different distribution of the incidence of tetanus has been observed depending on geographical areas.

IN Europe, the lowest overall incidence is observed in the Scandinavian countries (0.05 per 100,000 inhabitants). And the highest (more than 0.5 per 100,000 inhabitants) on about. Malta and Portugal. The next places are occupied by Greece, Spain, the Netherlands, etc. descending.

As for the former USSR, the highest prevalence is observed in the republics of Central Asia and in Kazakhstan.

IN In the Republic of Belarus, the incidence of tetanus is currently recorded in the form of isolated cases.

Etiology. The causative agent of tetanus is Clostridium tetani, Fisher's bacillus, a gram-positive bacillus, a strict anaerobe, forms terminal spores, does not produce lipases, urease, does not restore nitrates.

Vegetative forms of the pathogen synthesize tetanospasmin, a toxin that acts on human neurons. Most strains of tetanus bacillus produce oxygen-labile tetanolysin, which is able to dissolve the patient's red blood cells.

Vegetative forms of tetanus bacillus are not resistant to the action of damaging environmental factors. Boiling (100 C) destroys the pathogen and even at 80 C for 30 minutes they die. Most disinfectants cause the death of vegetative forms.

But tetanus bacillus spores, on the contrary, are very resistant to environmental factors. So, when boiled, they die only after 1 hour, in disinfecting media they die only after 10-12 hours, and in the soil they can persist for many years (up to 30 years).

Epidemiology

The source of the infectious agent are animals and humans, in the intestines of which the pathogen saprophytes. Tetanus bacillus is found in the intestines of horses, cows, pigs, and sheep. With faeces, the pathogen enters the environment, and from there through the wound surface into the human body. This is a typical wound infection (combat, industrial, household injuries, including burns). This disease was once called the disease of bare feet. To get sick or not to get sick - it all depends on the presence or absence of immunity.

The entrance gate of the causative agent of tetanus can be both significant and barely noticeable wounds.

The incidence of tetanus increases dramatically during wars. Pathological semiotics in tetanus has no characteristic

features and does not correspond to the severe clinical picture of the disease. Clinic. The incubation period for tetanus lasts for

7-14 days. Sometimes the disease can occur within a few hours to one month. The shorter the incubation period, the more severe the tetanus and the worse the results of treatment. According to the severity of the course, very severe, severe, moderate and mild forms of tetanus are distinguished.

In the prodromal period, general weakness, increased irritability, pulling pains in the wound, fibrillar twitching of the muscles adjacent to the wound may disturb.

The earliest and most characteristic symptom of tetanus is trismus - reduction of the jaws as a result of tonic spasm of the masticatory muscles (m. masseter). As a result, the patient cannot open his mouth. The next sign of tetanus is the "sardonic smile" - wrinkled forehead, narrowed palpebral fissures, stretched lips and downturned corners of the mouth. Difficulty swallowing (dysphagia) occurs due to spasm of the muscles of the pharynx. It's early

symptoms, their combination (triad) is characteristic only for tetanus.

Later, there is a tonic contraction of other muscle groups - the occipital, long muscles of the back, muscles of the limbs. The hypertonicity of these muscles leads the patient to a typical position: on the back with the head thrown back and the lumbar part of the body raised above the bed. The patient arches and, as it were, stands on the back of the head and heels - the so-called epistotonus. Somewhat later, tension of the abdominal muscles appears - a board-shaped abdomen, as with a perforated ulcer. Further, the muscles of the limbs are tensed and their movements are sharply limited. Due to the involvement of the intercostal muscles in the process, chest excursion is limited, breathing becomes shallow and frequent.

Due to the tonic contraction of the muscles of the perineum, urination and defecation become difficult. In the future, against the background of general muscle hypertonicity, general tonic convulsions appear. Often during convulsions, patients bite their tongue, which is also a diagnostic feature.

With a very severe form of tetanus, paralysis of the respiratory muscles occurs, which leads to death.

Tetanus is characterized by an increase in body temperature, sometimes significant, there is constant sweating. Hypersalivation is noted - constant salivation.

IN Consciousness is preserved throughout the illness. Patients are irritable - the slightest noise or light leads to an attack of convulsions.

IN cases of a favorable outcome, the clinical picture stops within 2-4 weeks. Muscles hurt for a long time. Relapses of the disease are rare.

The diagnosis is based on the history, characteristic clinical picture and laboratory results. For laboratory analysis, material is taken from wounds and inflammatory formations and blood. Produce crops in an anaerobic environment with subsequent identification of the microbe. Differential diagnosis is made with diseases such as epilepsy, hysteria, meningitis, encephalitis and others accompanied by convulsive syndrome.

Treatment: patients are hospitalized in intensive care units. Light and noise irritants are excluded. Surgical treatment of wounds must be performed under anesthesia, the wounds are not sutured. A radical excision of the edges of the wound is carried out, its treatment with oxygen-releasing antiseptics and sufficient drainage of the wound is ensured.

In order to prevent the entry of tetanus toxin from the wound into the blood, before treating the wound, it is advisable to “chip” it with antitetanus serum at a dose of 5-10 thousand IU. Mandatory surgical treatment under anesthesia - do not provoke convulsions.

Specific treatment consists in the intramuscular injection of 50100 thousand IU of tetanus toxoid after testing for

sensitivity of the body to a foreign protein. This amount of serum provides a high antitoxic titer in the patient's blood for 2-3 weeks. In this connection, there is no need for re-introduction. Anti-tetanus serum is administered after the test according to the Bezredko method intramuscularly, and only in especially severe cases, in parallel with intramuscular injection, intravenous slow administration of sodium chloride diluted with an isotonic solution 5 times is used. Intravenous administration of PPS

lasts 2-3 days. Serum should be warmed up to

36-37o C.

IN Recently, anti-tetanus human immunoglobulin, which is administered intramuscularly at a dose of 900 IU (6 ml), has a more pronounced antitoxic effect. To stimulate active immunity in the acute period of the disease, 1.0 ml of tetanus toxoid is administered.

Convulsive muscle contraction in mild and moderate forms of tetanus is stopped after the introduction of neuroleptics (aminosine, droperidol) or tranquilizers (seduxen). In severe forms of the disease, hexenal, thiopental, sodium hydroxybutyrate, sombrevin are additionally administered.

IN in especially severe cases, patients are intubated with periodic administration of muscle relaxants and artificial ventilation of the lungs.

All possible methods of detoxification of the body and symptomatic treatment are used. Tube or parenteral nutrition. Antibiotics are required to prevent pyogenic infection. A good effect is the treatment of patients under high oxygen pressure. Hyperbaric oxygenation (HBO) is carried out by placing patients in a pressure chamber, where the oxygen pressure is two atmospheres.

The prognosis is most often favorable, the mortality rate is 10-15%. Prevention. nonspecific and specific. Nonspecific

prevention consists in observing asepsis and antisepsis, in conducting primary surgical treatment of wounds.

Specific prophylaxis of tetanus begins to be carried out for all children, starting from 3 months of age. For this, the associated pertussis, diphtheria and tetanus vaccine (DPT) is used. The vaccine is administered three times at 0.5 ml with an interval of 1.5 months. Revaccination is performed once every 1.5-2 years. Maintaining immunity at the proper level is ensured by the introduction of 0.5 ml of ADS at the age of 6, 11, 16 years and beyond every 10 years of life.

If a fully vaccinated person is injured, then only 0.5 ml of toxoid is shown to him. In cases of injury, previously unvaccinated patients are given 450-900 ml of tetanus immunoglobulin. In its absence, it is necessary to introduce 3000 IU of tetanus toxoid and 1.0 ml of tetanus toxoid.

Anaerobic gas infection

Anaerobic gas infection is a formidable wound infection,

caused by pathogenic anaerobes, characterized by rapidly advancing and spreading tissue necrosis, their decay, usually with the formation of gases, severe general intoxication and the absence of pronounced inflammatory phenomena.

Other names for the disease: gas gangrene, gas phlegmon, anton fire, malignant edema, fulminant gangrene, brown phlegmon, etc.

History. The first description of the clinical manifestations of anaerobic infection belongs to Hippocrates. Subsequently, a fairly detailed description of anaerobic infection of soft tissues was made by the French physician Ambroise Pare (1562), who considered it to be hospital gangrene. A great contribution to the doctrine of gas gangrene was made by N.I. Pirogov, during World War II S.S. Yudin, M.N. Akhutin.

Etiology: three main pathogens: Cl. perfringens, Cl. septicum, Cl.

aedemaitiens. the most common cause of anaerobic infection is Cl. perfringens, it is divided into 6 types according to their ability to produce 12 different lethal and necrotic toxins and enzymes.

Other clostridia are also divided into several types (see microbiology).

Two more pathogens are attached to these three pathogens - this is Cl. hystolyticum and Cl. sordelli is the first not pathogenic for humans, but in combination with others, it enhances the pathogenic properties of each other and can be the cause of death. Cl. sordellii is more toxic and is capable of releasing a deadly toxin.

Epidemiology. The natural habitat of anaerobes is the intestines of animals, especially herbivores (cow, horse), as well as omnivores (pig). In the intestine, they multiply as saprophytes without causing disease in the animal. From the intestines of animals, anaerobes enter the soil. If a wound of any origin is contaminated with soil, then anaerobes, getting from the soil, seed the wound surface.

conditions for the development of the disease. Many wounds can be contaminated with anaerobic microorganisms, but the disease does not occur in all cases. For the development of anaerobic infection, the following conditions or so-called local factors must be present. These include:

- a large volume of necrotic and insufficiently oxygenated tissues;

- the presence of traumatic and hemorrhagic shock;

- extensive crushing and damage to muscles and tissues;

- deep wound channel;

- wound surface closed from the external environment;

- tissue ischemia as a result of injury to the main arteries;

- decrease in body resistance.

Pathogenesis. Under favorable conditions and in the absence of body resistance, the presence of a suitable nutrient medium, anaerobes, after penetrating into tissues, begin to multiply and develop their destructive activity. From the wound, clostridia penetrate into healthy

areas, damage tissues with their toxins and thereby prepare a suitable nutrient medium for themselves. The process proceeds especially rapidly in muscle tissue, because. due to its rich glycogen content, it is the best nutrient medium. Another place of localization of microbes is the connective tissue. In the action of anaerobes and their toxins, three phases can be distinguished:

1) swelling and fluid filling, followed by a characteristic coloration of the skin;

2) gas formation in muscles and connective tissue;

3) necrosis and softening of the muscles from which gas escapes.

Edema and gas, squeezing healthy tissues, lead to disruption of microcirculation and cause ischemia with subsequent cell death. Necrotic and ischemic tissues are further attacked by anaerobes and more and more new areas are involved in the process.

Characteristic changes occur in the color of the skin. In the initial stage, the skin is always pale (toxins cause vasospasm). As a result of swelling and gas formation, the skin becomes shiny. A distinctive feature from a banal (aerobic) infection is that there is no hyperemia of the skin. There is also no hyperthermia of the skin, on the contrary, it is cold to the touch. The saphenous veins are dilated, overflowing with blood, tense (as when a tourniquet is applied). As the process progresses, the skin acquires a bronze tint, later green, brown and then black.

Muscle tissue: Under the influence of a gas infection, the muscles at first become pale red, dry (kind of boiled meat), they are filled with gas bubbles. Subsequently, the color of the muscles becomes brown or black with a greenish tint. Subsequently, the muscle tissue turns into a black-brown mass, from which gas is released.

General phenomena

Gas gangrene, in whatever form it takes, never goes locally. From the very first hours of the disease, the whole organism is involved in the process. Anaerobic pathogens act mainly with their strong toxins, which flood the entire body and poison the body very quickly. With a lightning-fast course, death can occur in just a few hours.

The general condition of the patients is severe. However, their health is not always the same. Less commonly, patients are in a depressed mood. More often they have a pronounced euphoria. Attention is drawn to the pronounced talkativeness of patients and their excitement. They willingly answer questions and give soothing answers, they never complain about their condition. They almost never realize the severity of their disease, they do not agree to amputation, they say that they feel good. Sleep in patients with gas gangrene is completely absent. Even under the influence of sleeping pills, patients do not sleep. Body temperature - 38-39. Pulse - 140-150 in one minute. BP 80-90 mm. rt. Art. Breathing quickened. Leukocytosis - pronounced, shift of the formula to the left,

in the terminal stage - the content of hemoglobin, erythrocytes quickly decreases, anisoditosis, hypochelomia appears (since anaerobes destroy erythrocytes and inhibit hematopoiesis). There is oligo - or anuria.

Classification

Classification of anaerobic infection according to the rate of spread: 1 - rapidly spreading or fulminant; 2 - slowly spreading.

According to clinical and morphological indicators: 1 - gas form, 2 - edematous form, 3 - gas-edematous, 4 - putrefactive-purulent form.

According to anatomical features: deep, superficial.

Diagnosis: Anyone who has ever observed an anaerobic infection, unwittingly came to the conclusion about the importance of early diagnosis of this disease. With a late diagnosis, the prognosis becomes doubtful. Those. early diagnosis forms the basis for reducing mortality and disability. It becomes obvious knowledge of the clinic of this formidable disease. What is the diagnosis based on?

The first signal of a possible disaster is pain in the wound. With gas gangrene, the pain in the wound is so severe that it is not stopped even by drugs.

The next early sign is tissue swelling in the wound area. It is easy to identify it using the symptom of A.V. Melnikov. The symptom is positive if the ligature, tightly applied above the wound, begins to cut into the skin within one hour, which indicates an increase in the volume of the limb.

The following symptoms are signs of intoxication - primarily euphoria, hyperthermia, tachycardia.

Local symptoms - "white" edema - anaerobic bacteria secrete a toxin, which causes a sharp narrowing of blood vessels in the tissues. As a result, the skin becomes pale and cold to the touch (as opposed to a banal infection, where the skin is hyperemic and hot to the touch). Subsequently, due to the development of edema and accumulation of gases, the skin becomes shiny. These changes taken together made it possible in some cases to call gas gangrene a white face. An undoubted sign is the definition of subcutaneous emphysema in the form of crepitus. Percussion tympanitis.

The wound, despite the swelling, is usually dry, only when pressed, a transparent red odorless liquid separates from it, with glitters of fat that floats in it, like in broth, sometimes the wound discharge is foamy. In the future - tissue necrosis around the wound. R-graphy of the extremities is used to detect gas in the muscles. In the R-image: gas in the muscles has a herringbone pattern, and the accumulation of gas in the subcutaneous tissue has the appearance of a honeycomb. But this research method should not be overestimated. Gas gangrene is characterized by a putrid pungent odor that comes from a bandage applied to the wound.

As you know, O. Balzac died of gas gangrene. Here is how it describes

Victor Hugo his last meeting with O. Balzac: “I called. The moon shone, darkened by clouds. The street was deserted. I called again. A maid appeared with a candle. What do you want? She cried. I identified myself and was shown into the living room. A candle burned in the middle of the room. Another woman came in, she was also crying. She told me: “He is dying. The doctors have abandoned him since yesterday.” We went to Balzac's bedroom. I heard an ominous snoring. An unbearable smell emanated from the bed. I lifted the blanket and took Balzac's hand. She was cold and damp with sweat. He didn't respond to the pressure. When I arrived home, I found several people waiting for me. I told them: gentlemen, Europe is now losing a genius.

Microbiological diagnostics. For bacterial examination during the primary operation, exudate, pieces (2-3 g) of altered tissue are taken from a wound on the border with healthy tissue, as well as blood from a vein. The taken material is placed in a sterile hermetically sealed glassware and sent to the bacteriological laboratory. Smears are prepared, Gram-stained, and microscoped. The presence of gram-positive rods in the sample serves as an indicative sign of an anaerobic infection. The next study is the sowing of the taken material on a medium of a special composition and incubation under anaerobic conditions. Determination of the type of pathogen produced in 24-48 hours, up to 7 days. In addition, the determination of the type of pathogen and its toxin is carried out by a neutralization reaction with antitoxic diagnostic sera to all pathogens.

There are a number of methods of accelerated diagnostics.

Complex. Surgical treatment is the main one and should be carried out on an emergency basis. Excision - dissection of tissues should be combined with excision: the wound should be wide open, after which it is necessary to perform a complete, sometimes very extensive, excision of all affected muscles (gray, non-bleeding). The criterion for muscle viability is the contraction of muscle bundles.

In the presence of a fracture, the application of a circular plaster cast or the use of metal osteosynthesis is contraindicated. In these cases, skeletal traction or a plaster splint is used. The wound area must be left open so that dressings can be made.

Locally, for the treatment of wounds, solutions such as 10-20% NaCl, hydrogen peroxide, potassium permanganate are used - it is necessary, since they are oxidizing agents, contain O2, dioxidine, dimexide, antibiotic solutions.

Specific treatment is carried out - intravenous administration of polyvalent antigangrenous serum. 150,000 IU (50,000 IU antiperifrengens, antisepticum, antioedematiens) of serum are administered per day, which is diluted 3-5 times with saline. After identification of the causative agent, only 50,000 IU of a similar serum is administered intravenously.

Massive antibiotic therapy is carried out. Preference should be given to antibacterial drugs such as clindomycin, beta-lactamase inhibitors (amoxicillin, etc.), carbapenems (meropenem, thienem). The chemotherapy drug metronidazole is very effective.

It is desirable to combine the treatment with hyperbaric oxygen therapy.

All available methods of detoxification are used.

At present, suppuration caused by non-spore-forming anaerobes has become a fundamentally new problem of purulent infection.

In 1861-1863, Pasteur was the first to describe the possibility of bacteria developing without air. The discovery of anaerobiosis and the study of a number of anaerobic bacteria - the causative agents of surgical diseases and purulent complications already at the beginning of the 20th century made it possible to identify Three groups anaerobic infections. First - Botulism and tetanus Second- clostridial gangrene of soft tissues. Due to their characteristic clinic and characteristics of pathogens, they were considered specific infections, which make up an insignificant proportion in the general list of human anaerobic infections. The third group -"banal" purulent putrefactive processes, occurring, as a rule, with the participation of non-spore anaerobes, it constitutes the most significant category of purulent-inflammatory diseases.

In 1898, \7eilon and Libre, while examining pus from the abdominal cavity in a patient with destructive appendicitis, for the first time discovered anaerobic bacteria that differed from the causative agents of gas gangrene. During this period, researchers managed to prove the presence of asporogenic obligate anaerobes in surgical infections of various localizations, as well as clarify their main habitat in the human body.

However, the technique of working with anaerobes was very difficult, and anaerobes in abscesses were often accompanied by aerobes. As a result, the study of infection has not become as deep as one would like, although clinical microbiology was born as microbiology of aerobes and anaerobes equally.

Clinicians showed considerable attention to non-spore-forming anaerobes in the late 1960s, when methods for cultivating, isolating, and identifying non-spore-forming anaerobes were improved at the Virginia Polytechnic Institute. Advances in laboratory technology allowed Moore already in 1969 to establish that non-spore-forming anaerobes were found in bacteriological examination of the material in 85% of cases. Thus, the predominance of asporogenic anaerobes in purulent infection over all other potential pathogens was proven for the first time.

In our country, the priority in the study of anaerobic infections in humans belongs to the St. Petersburg Military Medical Academy (Kolesov A.P., Stolbovoy A.V., Borisov I.V., Kocherovets V.I.) and the Institute of Surgery. A. V. Vishnevsky (Kuzin M. I., Kostyuchenok B. M., Kolker I.. I., Vishnevsky A. A., Shimkevich L. L., Kuleshov SE. and others).

The modern stage in the study of infection is rightly considered the epoch of the revival of the doctrine of anaerobes, which are called the "forgotten" microflora.

Etiology and pathogenesis. It has now been established that non-spore-forming anaerobes are the causative agents of purulent infection from 40 to 95% of observations (Kolesov A. P. et al., 1989; Kuzin M. I. et al., 1990; Kocherovets V. I., 1991; Bezrukov V. M., Robustova T.T., 2000; Leshchenko IT., 2001; Sharogorodsky A.T., 2001; Finegold S.M., 1980; Bachetal M., 1988; Maddaus M. et al., 1988).

Most anaerobic non-spore-forming bacteria are moderate anaerobes, that is, they tolerate the presence of oxygen at a concentration of 0.1-5%. They live in the oral cavity, digestive tract, nasopharynx, genitals, and on the human skin. Currently, representatives of non-spore-forming anaerobic microorganisms of the following genera are known (Finegold S. M., 1977):

Gram-positive anaerobic cocci: Ruminicoccus, Peptococcus, Peptostreptococcus;

Gram-negative anaerobic cocci: Veilonella, Arachnia;

Gram-positive anaerobic bacteria: Actinomyces, Lactobacillus, Bifidobacterium, Eubacterium;

Gram-negative anaerobic bacteria: Bacteroides, Fusobacterium, Butyrivibrio, Campylobacter.

These genera of asporogenic anaerobes include up to several dozen species of pathogens, which may differ in morphological features, pathogenic properties, and the degree of sensitivity to chemotherapy agents.

According to the results of domestic and foreign studies, it was found that the microflora of purulent foci is polymicrobial in nature and is presented in the form of associations. At the same time, non-clostridial anaerobes prevail in the etiology of dental infection (Kocherovets V.I., 1990; Vgook I., 1988).

Often, the aerobe-anaerobe association exhibits synergism. This is confirmed by clinical observations. Thus, the association of microbial species that are slightly pathogenic in isolation often causes severe infectious lesions that occur with a pronounced destructive-necrotic process and sepsis (Stolbovoy A. B., 1981; Kolesov A. P. et al., 1989).

An increase in the pathogenicity of aerobes in the presence of facultative anaerobic microorganisms has been proven. At the same time, the combination of various types of bacteroids and fusobacteria with Escherichia coli, Proteus, aerobic coccal microflora is the most typical (Borisov V.A., 1986; Kocherovets V.I., 1990; Leshchenko IT., 2001). This statement is also confirmed by our study (I. G. Leshchenko, V. C. Novokshenov, 1993), in which 180 sick with purulent infection of various localization using aerobic-anaerobic microbiological techniques. The data obtained showed that purely aerobic microflora was isolated in 33.9% of clinical observations, mixed aerobic-anaerobic microflora - in 37.2%, non-clostridial anaerobic microflora - in 20%. In 8.9% of cases, anaerobic clostridia were sown in combination with other microbes. However, in all cases of detection of anaerobic clostridia, this was not clinically manifested. It was found that the main causative agents of anaerobic non-clostridial infection (ANI) are bacteroids (38.3%), peptostreptococci (27.3%) and peptococci (17.8%). Other genera of asporogenic anaerobes are isolated much less frequently - from 0.8 to 2.3%. The frequency of manifestation of ANI depends on the nature and localization of the inflammatory process and ranges from 33.3% in post-traumatic soft tissue inflammation to 77.8% in purulent soft tissue infection faces and neck.

The pathogenesis of anaerobic non-clostridial and mixed infections is determined by three interdependent factors:

Localization of the introduction of infection;

The type of pathogen, its pathogenicity and virulence;

Immunological and nonspecific reactivity of the body.

The conditions noted above create an opportunity for the appearance of non-clostridial anaerobes in unusual habitats. More often, ANI develops near mucous membranes, when bitten by a person or animal.

The pathogenetic mechanisms of endogenous infections caused by non-spore-forming anaerobes have not yet been sufficiently studied. Their pathogenicity is presumably associated with the presence of toxic polysaccharides and proteins in them. The formation of capsules in some types of bacteroids is considered as a pathogenetic feature (Ezepchuk Yu. V., 1985; Tabachaji S. et al., 1982; Brook I. et al., 1983).

Certain importance in the pathogenesis of diseases caused by asporogenic anaerobes may have enzymes that ensure their tolerance to tissue oxygen and the environment; superoxide dismutase and catalase (Bergan T., 1984; Bjornson A., 1984), as well as enzymes that provide resistance to antibiotics(Tajama T. et al, 1983).

Bacteroides have been found to be able to protect other types of bacteria that are in association with them from the action of antibiotics (Brook I. et al., 1983). This is of clinical importance, as it reveals the reason for unsuccessful antibiotic therapy in mixed infections involving bacteroids.

ANI proceeds, as a rule, against the background of secondary immunodeficiency - suppression of cellular and humoral immunity (Vasyukov V. Ya., 1974; Korolyuk A. M. et al., 1983; Glynn A., 1975). At the same time, a decrease in the absolute and relative number of T-lymphocytes, a decrease in the concentration of immunoglobulins and complement are recorded. Depression of the opson-phagocytic system and destruction of leukocytes are noted.

Clinic. Due to the difficulties in organizing microbiological studies in wide dental practice, the basis for the diagnosis of ANI is clinical symptoms.

Since ANI infection occurs by autoflora, an important clinical feature is the occurrence of inflammation near the natural habitats of anaerobes. With an infection of the soft tissues of the face and neck, such places may be the mucous membrane of the mouth.

The most typical clinical picture of ANI develops when soft tissues are affected by the type of diffuse inflammation without borders - phlegmon. At the same time, the skin is changed to a lesser extent. The infectious process develops, as a rule, in the subcutaneous fatty tissue (cellulitis), in the fascia (fasciitis), in the muscles (myositis). Both all these anatomical formations, and predominantly one of them, can be subject to inflammation.

Ulcers, in the formation of which anaerobes take part, are characterized by a deep location. Local classic signs of soft tissue inflammation in this regard are mild, which, as a rule, does not correspond to the manifestation of general symptoms of infection. This also explains the discrepancy between inflammatory changes in the skin and extensive damage to the underlying tissues: subcutaneous adipose tissue, fascia, muscles. At the same time, there may sometimes be dim spots on the skin that are sharply painful on palpation - "tongues of flame" (Salsky Ya.P., 1982).

From a purulent wound, an intense fetid putrid odor is released, which most surgeons tend to attribute to the vegetation of Escherichia coli. However, back in 1938, W. Altemeier showed that this odor is specific to anaerobes (quoted: according to Kolesov A.P. et al., 1989). In this regard, Tally and Gorbach (1977) note that although the smell is a pathological sign, it may be absent in 50% of cases of anaerobic infections.

The meager serous exudate discharged from the wound often has a gray or dark gray color, contains droplets of fat and fragments of necrotically altered tissues. If the exudate contains blood, then its color may be intensely black.

The presence of gas in soft tissues is characteristic of bacteroids, anaerobic streptococci, and corynebacteria. As a rule, it is not as pronounced as with clostridial infection. Before opening a purulent focus, gas formation can be confirmed radiologically, since crepitus, as a sign of gas formation, is rarely determined. In the first days after the onset of ANI, it is often possible to detect subictericity of the sclera and skin due to absorption of microbes and their toxins from the wound, hemolysis of erythrocytes, and toxic damage to the liver (Smit et al., 1970).

Careful examination of the wound can determine the area affected by the infection. Non-clostridial necrotic cellulitis is characterized by fusion of fatty tissue without a tendency to abscess formation. However, with a concomitant staphylococcal infection, the subcutaneous tissue on the cut resembles "purulent honeycombs". With a limited process, the skin over the focus of inflammation was changed slightly. If extensive damage to the underlying tissues occurs, then skin necrosis occurs due to a violation of its nutrition. With the transition of the process to the fascial sheaths, the fascia acquires a dark color, perforation of the structure due to its lysis. Scraps of necrotically altered fascia appear in the exudate.

With the development of infection in the muscles, they become swollen, flabby, gray-red in color, dull. On the incision, they do not bleed, while extensive yellowish areas of easily torn tissue, saturated with serous-hemorrhagic discharge, are determined.

With muscle damage, it is necessary to conduct a differential diagnosis between API and clostridial myositis. It should be remembered that it is characterized by an acute onset of the disease, severe local pain that does not go away even after the administration of narcotic analgesics. Muscles have the color of boiled meat, quickly swell and protrude from the wound, are easily destroyed when touched with tweezers, are saturated with scanty brown exudate. The appearance of the wound and surrounding tissues, in contrast to API, usually allows one to draw a conclusion about the depth and extent of the pathological process.

The next characteristic feature of ANI is a pronounced slowdown in the phases of the wound process - suppuration and cleansing. So, the suppuration phase with a spontaneous course lasts 2-3 weeks. Mild macrophage reaction leads to ineffective wound cleansing. Reparative processes are slowed down due to secondary suppuration of granulations and their death (Kuleshov S. S., Kaem R. I., 1990).

Thus, the local clinical signs of anaerobic non-clostridial infection are:

The discrepancy between mild classical signs of inflammation on the skin and extensive damage to the underlying tissues: subcutaneous tissue, fascia, muscles; a fetid putrefactive odor is released from a purulent wound;

The discharge from the wound is scanty, gray or dark gray, contains droplets of fat and fragments of necrotically altered tissues;

Sometimes there is gas in the tissues;

Non-clostridial necrotic cellulitis is characterized by fusion of fatty tissue;

With the transition of the process to the fascial sheaths, the fascia acquires a dark color, perforation of the structure due to its lysis. Scraps of necrotically altered fascia appear in the exudate;

With the development of infection in the muscles, they become swollen, flabby, gray-red in color, dull; on the cut they do not bleed, with extensive yellowish areas of easily torn tissue, saturated with serous-hemorrhagic discharge. Surgeons with extensive experience in the treatment of patients with ANI argue that the registration of even two of the above clinical signs gives grounds for diagnosing nonclostridial inflammation (Kolesov A.P. et al., 1989; Kuzin M.I. et al., 1990 ; Leshchenko I. G., Novokshenov BC, 1993).

General reaction organism with ANI, it manifests itself as a toxic-resorptive fever due to the absorption of tissue decay products and microbes, their toxins from the wound. Its signs: malaise, headache, chills, fever, in severe cases, blackout or complete loss of consciousness, motor agitation, delirium. The severity of these symptoms depends on the extent of tissue damage, the characteristics of the purulent wound and the usefulness of the surgical treatment.

Diagnostics. As can be seen, some features are characteristic of the clinical manifestation of ANI. However, the specificity of the symptom complex is still leveled by the fact that anaerobic non-clostridial monoinfection is relatively rare (1.3–20%), while a mixed aerobic-anaerobic infection is usually observed (up to 60%). In these cases, clinical diagnosis cannot have an independent, leading value. Moreover, it does not imply the establishment of an etiological diagnosis necessary for the organization of an effective antibacterial therapy.

The leading role in the recognition of API, of course, belongs to laboratory microbiological research methods. Among such diagnostic methods as microscopic, bacteriological, immunological, biological, chromatographic, not all have found practical application in the recognition of API.

In everyday clinical practice, for the rapid diagnosis of API, preference is given to microscopy of a Gram-stained wound discharge smear and gas-liquid chromatography. The use of bacterioscopy of purulent exudate allows, after 10-15 minutes, to roughly judge the microflora involved in suppuration. However, most ANI pathogens lack morphological features that allow them to be differentiated from aerobic and facultative anaerobic bacteria belonging to the same genus. The information content of the microscopic method is significantly increased when using a modification of the smear color according to Kopelov (Kocharovets V.I. et al., 1986). The coincidence of the results with bacteriological cultures in the diagnosis of gram-negative anaerobes was noted in 72.7% of cases (Kolker II et al., 1990).

Ultraviolet irradiation of a native smear makes it possible to identify B. melaninogenicus by the characteristic luminescence of the colonies. When performing gas-liquid chromatography, volatile fatty acids specific to anaerobic microbes are found in the test material. The practical significance of chromatographic analysis, which takes about 60 min, is great, despite the fact that not all asporogenic anaerobes form volatile fatty acids during metabolism. Currently, the gas-liquid chromatography method provides confirmation of the clinical diagnosis in ANI of soft tissues from 5 to 58% (Kuzin M. I. et al., 1987; Shimkevich L. L. et al., 1986; Istratov V. G. et al., 1989).

The percentage of coincidence of the diagnosis of ANI with the simultaneous use of chromatographic and bacteriological methods is quite high - from 52 to 97% (Korolev B. A. et al., 1986; Kuzin M. I. et al., 1987; Ponomareva T. R., Malakhova V. A., 1989).

However, the main method of etiological diagnosis of ANI is Bacteriological. Despite the fact that it remains technically complex and lengthy, only this method, based on the combined consideration of the various properties of pathogens, allows the most accurate and complete determination of the etiological structure of inflammation.

For specialized medical institutions with full-time anaerobic diagnostic laboratories, multi-stage bacteriological diagnostics is acceptable (Bochkov I. A., Pokrovsky V. I., 1983; Kolker I. I., Borisova O. I., 1990).

The first stage of microbiological research is the selection, collection and delivery of the test material, which are carried out in compliance with certain rules. The time elapsed between the collection of material and its cultivation should be minimal.

The second stage - microscopic examination of a native Gram-stained smear - makes it possible to draw a conclusion about the number of microorganisms and their gram-affiliation, which serves as a control for the subsequent isolation of anaerobes.

The third stage is the sowing of the test material on nutrient media, a common feature of which is the presence in them of reducing substances necessary to reduce the pH of the medium. A number of methods are used here:

1. Sowing culture by injection into a tall column of sugar agar.

2. Removal of air from the vessel by pumping out (use of various types of anaerostats).

3. Replacing air with an indifferent gas (the composition and ratio of gas mixtures may be different).

4. Mechanical protection against air oxygen (Vignal-Veillon method).

5. Chemical absorption of atmospheric oxygen (for example, with an alkaline solution of pyrogallol).

The fourth stage is the cultivation of anaerobic bacteria. It should be taken into account that different types of anaerobes grow at different rates.

The fifth stage is the isolation of pure culture.

The sixth stage is the identification of anaerobic bacteria. It is based on the study of cell morphology and its cultural characteristics, biochemical reactions (using modifications of the AP and Minir. ec systems), motility, ability to sporulate, sensitivity to antibiotics, pigment production, etc. Identification of anaerobes by determining their fermentation products is carried out using gas chromatographs, while the period of diagnosis does not exceed 1 hour. A promising method is the identification of anaerobic bacteria using a computer. KeHey and Ke1^ developed a computer program that included 28 genera and 238 species of anaerobes, including biochemical and chromatographic tests. The system is designed for fast, accurate and high-performance recognition of unknown crops. Identification time from a few seconds to 40 minutes.

These methods are complex and time-consuming, require special equipment and qualifications of medical personnel. Therefore, the problem of developing domestic express methods and systems that provide timely diagnostics and adequate treatment diseases caused by anaerobic bacteria.

In this regard, our joint eight-year scientific and practical research (the Department of Military Field Surgery of the Samara Military Medical Institute and the Department of Microbiology of the Samars Kogo State Medical University) ended with the development of a new nutrient medium for the cultivation of both aerobes and anaerobes (Buchin P. I. and et al., 1989). Glucose indicator agar, produced by the Makhachkala Research Institute of Nutrient Media, was used as the basis of this medium. Our fellow microbiologists have developed, tested and patented a thermostable, transparent stimulator of microbial growth of asporogenic anaerobes. The drug is prepared on the basis of microbial blood milk hydrolyzate and contains a number of other growth substances. It is heat-resistant, sterilized in an autoclave at 0.5 atm for 30 minutes. Stored in the refrigerator. It is added to the glucose indicator agar as 10-15% of the medium, which has a transparent purple color, and under sterile conditions it is poured into Vinyal tubes.

Aerobic pyogenic bacteria, as well as anaerobes-peptococci, peptostreptococci develop on artificial nutrient media. Bacteroides (obligate anaerobic gram-negative rod-shaped bacteria) are characterized by slow growth. In this regard, a visual assessment of the results of inoculation of the test material in the Vinyal tube is carried out daily for five days (the deadline for observation), and for a beveled medium - for three days (the deadline for observation), until the first signs of the development of a microbial culture appear. This is evidenced by a change in the color of the indicator nutrient substrate, as well as the formation of microscopic colonies in the thickness of the medium, which are easily distinguishable under a low magnification of the microscope (objective 10x) when microscopy of tubes and test tubes from the bottom of the sloping substrate layer.

The development of all asporogenic anaerobic pathogenic bacteria fermenting the carbohydrates contained in the nutrient medium to acid is characterized by a change in the color of the substrate from the original purple to yellow without the appearance of gas bubbles in the thickness of the medium. Pronounced gas formation against the background of yellowing of the medium in the tube is typical for anaerobic clostridia (potential causative agents of gas gangrene), as well as some facultative anaerobic bacteria, if the latter germinate under strictly anaerobic conditions.

For the growth of staphylococci, streptococci and proteus on a slant medium in a test tube, the color of the substrate changes from the original purple to yellow, for Pseudomonas aeruginosa - from purple to blue. Escherichia are characterized by either the absence of a change in the purple color of the medium during massive growth, or yellowing of the substrate during sparse growth.

When comparing the results of inoculation of the material under study according to the Vinhal-Veyon method and on a sloping medium, it is necessary to be guided by the data given in Table. eleven.

Table 11

Evaluation of the results of aerobic-anaerobic seeding of the test material

Variant	Seeding result	Conclusion
	No evidence of microbial growth on the Viñal tube for five days, and on the slant in vitro for three days	Negative test result
	The presence of growth only in the Vinyal tube against the background of the absence of growth on slant medium in a test tube	Isolated culture - obligate anaerobe
	The presence of microbial growth in the Vinyal tube, as well as on the slant medium in the test tube with the same microbial morphology, according to the results of subsequent microscopic examination	Isolated culture - facultative anaerobe
	The presence of growth in the Vinyal tube, as well as on the slant medium in the test tube with different morphology of microbes, according to the results of subsequent microscopic examination	A mixed culture of anaerobe and aerobe is isolated
	Absence of growth in the Viñal tube against the presence of growth on the slant medium in the test tube	Isolated culture - aerobe General information. Furuncle - Acute purulent-necrotic inflammation of the hair follicle, surrounding tissues; According to the classification, it belongs to the group of deep […] The treatment of abscesses and phlegmons of the maxillofacial area and neck is complex, including the simultaneous effect on the purulent focus, […]

Anaerobic infection is a rapidly developing pathogenic process that affects various organs and tissues in the body and often leads to death. It affects all people, regardless of gender or age. Timely diagnosis and treatment can save a person's life.

What it is?

Anaerobic infection is an infectious disease that occurs as a complication of various injuries. Its pathogens are spore-forming or non-spore-forming microorganisms that develop well in an anoxic environment or with a small amount of oxygen.

Anaerobes are always present in the normal microflora, mucous membranes of the body, in the gastrointestinal tract and the genitourinary system. They are classified as conditionally pathogenic microorganisms, since they are natural inhabitants of the biotopes of a living organism.

With a decrease in immunity or the influence of negative factors, bacteria begin to actively multiply uncontrollably, and microorganisms turn into pathogens and become sources of infection. Their waste products are dangerous, toxic and rather aggressive substances. They are able to easily penetrate cells or other organs of the body and infect them.

In the body, some enzymes (for example, hyaluronidase or heparinase) increase the pathogenicity of anaerobes, as a result, the latter begin to destroy muscle and connective tissue fibers, which leads to microcirculation disorders. Vessels become fragile, erythrocytes are destroyed. All this provokes the development of immunopathological inflammation of blood vessels - arteries, veins, capillaries and microthrombosis.

The danger of the disease is associated with a large percentage of deaths, so it is extremely important to notice the onset of the infection in time and immediately begin its treatment.

Causes of infection

There are several main reasons why infection occurs:

• Creation of suitable conditions for the vital activity of pathogenic bacteria. This may happen:
• when an active internal microflora gets on sterile tissues;
• when using antibiotics that have no effect on anaerobic gram-negative bacteria;
• in case of circulatory disorders, for example, in the case of surgery, tumors, injuries, foreign bodies, vascular diseases, tissue necrosis.
• Infection of tissue by aerobic bacteria. They, in turn, create the necessary conditions for the vital activity of anaerobic microorganisms.
• Chronic diseases.
• Some tumors that are localized in the intestines and head are often accompanied by this disease.

Types of anaerobic infection

It differs depending on what agents it is provoked and in what area:

Surgical infection or gas gangrene

Anaerobic surgical infection or gas gangrene is a complex complex reaction of the body to the effects of specific pathogens. It is one of the most difficult and often untreatable complications of wounds. In this case, the patient is concerned about the following symptoms:

• increasing pain with a feeling of fullness, since the process of gas formation takes place in the wound;
• fetid smell;
• exit from the wound of a purulent heterogeneous mass with gas bubbles or inclusions of fat.

Tissue edema progresses very quickly. Externally, the wound acquires a gray-green color.

Anaerobic surgical infection is rare, and its occurrence is directly related to the violation of antiseptic and sanitary standards during surgical operations.

anaerobic clostridial infections

The causative agents of these infections are obligate bacteria living and multiplying in an anoxic environment - spore-forming representatives of clostridium (gram-positive bacteria). Another name for these infections is clostridiosis.

In this case, the pathogen enters the human body from the external environment. For example, these are such pathogens:

• tetanus;
• botulism;
• gas gangrene;
• toxicoinfections associated with the use of low-quality contaminated food.

A toxin secreted, for example, by clostridia, contributes to the appearance of exudate - a liquid that appears in body cavities or tissues during inflammation. As a result, the muscles swell, become pale, have a lot of gas in them, and they die.

Anaerobic non-clostridial infections

Unlike obligate bacteria, representatives of the facultative species are able to survive in the presence of an oxygen environment. The causative agents are:

• (spherical bacteria);
• shigella;
• escherichia;
• yersinia.

These pathogens cause anaerobic non-clostridial infections. These are more often purulent-inflammatory infections of the endogenous type - otitis media, sepsis, abscesses of internal organs and others.

In gynecology

The microflora of the female genital tract is rich in various microorganisms and anaerobes as well. They are part of a complex microecological system that contributes to the normal functioning of the female genital organs. Anaerobic microflora is directly related to the occurrence of severe purulent-inflammatory gynecological diseases, such as acute bartholinitis, acute salpingitis and pyosalpinx.

The penetration of anaerobic infection into the female body is facilitated by:

• injuries of the soft tissues of the vagina and perineum, for example, during childbirth, during abortions or instrumental studies;
• various vaginitis, cervicitis, cervical erosion, tumors of the genital tract;
• remnants of membranes, placenta, blood clots after childbirth in the uterus.

An important role in the development of anaerobic infections in women is played by the presence, intake of corticosteroids, radiation and chemotherapy.

Qualification of anaerobic infections according to the localization of its focus

There are the following types of anaerobic infections:

• Soft tissue and skin infections. The disease is caused by anaerobic Gram-negative bacteria. These are superficial diseases (cellulitis, infected skin ulcers, consequences after major diseases - eczema, scabies and others), as well as subcutaneous infections or postoperative ones - subcutaneous abscesses, gas gangrene, bite wounds, burns, infected ulcers in diabetes, vascular diseases. With a deep infection, soft tissue necrosis occurs, in which there is an accumulation of gas, gray pus with a vile odor.
• Bone infection. Septic arthritis is often the result of neglected Vincent, osteomyelitis - a purulent-necrotic disease that develops in the bone or bone marrow and surrounding tissues.
• Infections of the internal organs, including women, bacterial vaginosis, septic abortion, abscesses in the genital apparatus, intrauterine and gynecological infections may occur.
• Infections of the bloodstream- sepsis. It spreads through the bloodstream;
• Serous cavity infections- peritonitis, that is, inflammation of the peritoneum.
• bacteremia- the presence of bacteria in the blood, which get there in an exogenous or endogenous way.

Aerobic surgical infection

Unlike anaerobic infections, aerobic pathogens cannot exist without oxygen. Cause infection:

• diplococci;
• sometimes ;
• intestinal and typhoid coli.

The main types of aerobic surgical infection include:

• furuncle;
• furunculosis;
• carbuncle;
• hydradenitis;
• erysipelas.

Aerobic microbes enter the body through the affected skin and mucous membranes, as well as through the lymphatic and blood vessels. It is characterized by elevated body temperature, local redness, swelling, pain and redness.

Diagnostics

For a timely diagnosis, it is necessary to correctly assess the clinical picture and provide the necessary medical care as soon as possible. Depending on the localization of the focus of infection, various specialists are engaged in diagnostics - surgeons of different directions, otolaryngologists, gynecologists, and traumatologists.

Only microbiological studies can confirm for sure the participation of anaerobic bacteria in the pathological process. However, a negative answer about the presence of anaerobes in the body does not reject their possible participation in the pathological process. According to experts, about 50% of the anaerobic representatives of the microbiological world today are uncultivated.

High-precision methods for indicating anaerobic infection include gas-liquid chromatography and mass spectrometric analysis, which determines the amount of volatile liquid acids and metabolites - substances that form during metabolism. No less promising methods are the determination of bacteria or their antibodies in the patient's blood using enzyme immunoassay.

They also use express diagnostics. The biomaterial is studied in ultraviolet light. Spend:

• bacteriological seeding of the contents of the abscess or detachable part of the wound in a nutrient medium;
• blood cultures for the presence of bacteria of both anaerobic and aerobic species;
• blood sampling for biochemical analysis.

The presence of infection is indicated by an increase in the amount of substances in the blood - bilirubin, urea, creatinine, as well as a decrease in the content of peptides. Increased activity of enzymes - transaminase and alkaline phosphatase.

An x-ray examination reveals an accumulation of gases in a damaged tissue or body cavity.

When diagnosing, it is necessary to exclude the presence in the patient's body of erysipelas - a skin infectious disease, deep vein thrombosis, purulent-necrotic tissue lesions by another infection, pneumothorax, exudative erythema, frostbite stage 2-4.

Treatment of anaerobic infection

When treating, you can not do such measures as:

Surgical intervention

The wound is dissected, the dead tissue drastically dries up, and the wound is treated with a solution of potassium permanganate, chlorhexidine, or hydrogen peroxide. The procedure is usually performed under general anesthesia. Extensive tissue necrosis may require amputation of the limb.

Medical therapy

It includes:

• taking painkillers, vitamins and anticoagulants - substances that prevent clogging of blood vessels by blood clots;
• antibacterial therapy - taking antibiotics, and the appointment of a particular drug occurs after an analysis has been carried out for the sensitivity of pathogens to antibiotics;
• administration of antigangrenous serum to the patient;
• transfusion of plasma or immunoglobulin;
• the introduction of drugs that remove toxins from the body and eliminate their negative effects on the body, that is, they detoxify the body.

Physiotherapy

During physiotherapy, wounds are treated with ultrasound or laser. They prescribe ozone therapy or hyperbaric oxygenation, that is, they act with oxygen under high pressure on the body for medicinal purposes.

Prevention

To reduce the risk of developing the disease, a high-quality primary treatment of the wound is carried out in time, a foreign body is removed from the soft tissues. During surgical operations, the rules of asepsis and antisepsis are strictly observed. With large areas of damage, antimicrobial prophylaxis and specific immunization are carried out - prophylactic vaccinations.

What will be the result of the treatment? This largely depends on the type of pathogen, the location of the focus of infection, timely diagnosis and the right treatment. Doctors usually give a cautious but favorable prognosis for such diseases. In the advanced stages of the disease, with a high degree of probability, we can talk about the death of the patient.

Next article.