Diagnosis of anaerobic infection. Anaerobic infection
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Wound anaerobic infection attracts close attention of surgeons, infectious disease specialists, microbiologists and other specialists. This is due to the fact that anaerobic infection occupies a special place due to the exceptional severity of the disease, high mortality (14-80%), and frequent cases of profound disability of patients. Anaerobes and their associations with aerobes currently occupy one of the leading places in human infectious pathology.
Anaerobic infection can develop as a result of injuries, surgical interventions, burns, injections, as well as in the complicated course of acute and chronic purulent diseases of soft tissues and bones, vascular diseases against the background of atherosclerosis, diabetic angioneuropathy. Depending on the cause of the infectious disease of soft tissues, the nature of the damage and its location, anaerobic microorganisms are found in 40-90% of cases. Thus, according to some authors, the frequency of release of anaerobes during bacteremia does not exceed 20%, and with phlegmon of the neck, odontogenic infection, intra-abdominal purulent processes, it reaches 81-100%.
Traditionally, the term anaerobic infection applied only to infections caused by clostridia. However, in modern conditions, the latter are involved in infectious processes not so often, in only 5-12% of cases. The main role is given to non-spore-forming anaerobes. What both types of pathogens have in common is that they produce pathological effects on tissues and organs under conditions of general or local hypoxia using the anaerobic metabolic pathway.
ICD-10 code
A48.0 Gas gangrene
Pathogens of anaerobic infection
By and large, the causative agents of anaerobic infection include pathological processes caused by obligate anaerobes, which develop and exert their pathogenic effects under conditions of anoxia (strict anaerobes) or at low oxygen concentrations (microaerophiles). However, there is a large group of so-called facultative anaerobes (streptococci, staphylococci, Proteus, Escherichia coli, etc.), which, when exposed to hypoxic conditions, switch from aerobic to anaerobic metabolic pathways and are capable of causing the development of an infectious process clinically and pathomorphologically similar to a typical anaerobic one.
Anaerobes are ubiquitous. More than 400 species of anaerobic bacteria have been identified in the human gastrointestinal tract, which is their main habitat. In this case, the ratio of aerobes to anaerobes is 1:100.
Below is a list of the most common anaerobes, the participation of which in infectious pathological processes in the human body has been proven.
Microbiological classification of anaerobes
- Anaerobic gram-positive rods
- Clostridium perfringes, sordellii, novyi, histolyticum, septicum, bifermentans, sporogenes, tertium, ramosum, butyricum, bryantii, difficile
- Actinomyces israelii, naeslundii, odontolyticus, bovis, viscosus
- Eubacterium limosum
- Propionibacterim acnes
- Bifidobacterium bifidum
- Arachnia propionica
- Rothia dentocariosa
- Anaerobic gram-positive cocci
- Peptostreptococcus anaerobius, magnus, asaccharolyticus, prevotii, micros
- Peptococcus niger
- Ruminococcus flavefaciens
- Coprococcus eutactus
- Gemella haemolysans
- Sarcina ventriculi
- Anaerobic gram-negative rods
- Bacteroides fragilis, vulgatus, thetaiotaomicron, distasonis, uniformis, caccae, ovatus, merdae,
- stercoris, ureolyticus, gracilis
- Prevotella melaninogenica, intermedia, bivia, loescheii, denticola, disiens, oralis, buccalis, veroralis, oulora, corporis
- Fusobacterium nucleatum, necrophorum, necrogenes, periodonticum
- Porphyromonas endodontalis, gingivalis, asaccharolitica
- Mobiluncus curtisii
- Anaerorhabdus furcosus
- Centipeda periodontii
- Leptotrichia buccalis
- Mitsuokella multiacidus
- Tissierella praecuta
- Wolinella succinogenes
- Anaerobic gram-negative cocci
- Veillonella parvula
In the majority of pathological infectious processes (92.8-98.0% of cases), anaerobes are detected in association with aerobes and primarily with streptococci, staphylococci and bacteria of the Enterobacteriaceae family, non-fermenting gram-negative bacteria.
Among the many classifications of anaerobic infections in surgery, the classification proposed by A.P. Kolesov et al. should be considered the most complete and meets the needs of clinicians. (1989).
Classification of anaerobic infection in surgery
According to microbial etiology:
- clostridial;
- non-clostridial (peptostreptococcal, peptococcal, bacteroid, fusobacterial, etc.).
By the nature of the microflora:
- monoinfections;
- polyinfections (caused by several anaerobes);
- mixed (anaerobic-aerobic).
For the affected part of the body:
- soft tissue infections;
- infections of internal organs;
- bone infections;
- infections of serous cavities;
- bloodstream infections.
By prevalence:
- local, limited;
- unlimited, tending to spread (regional);
- systemic or generalized.
By source of infection:
- exogenous;
- endogenous.
By origin:
- out-of-hospital;
- intrahospital.
For reasons of occurrence:
- traumatic;
- spontaneous;
- Iatrogenic.
Most anaerobes are natural inhabitants of human skin and mucous membranes. More than 90% of all anaerobic infections are endogenous. Exogenous infections include only clostridial gastroenteritis, clostridial post-traumatic cellulitis and myonecrosis, infections after human and animal bites, septic abortion and some others.
Endogenous anaerobic infection develops when opportunistic anaerobes appear in places unusual for their habitat. Penetration of anaerobes into tissues and the bloodstream occurs during surgical interventions, injuries, invasive manipulations, tumor disintegration, and translocation of bacteria from the intestine during acute diseases of the abdominal cavity and sepsis.
However, for the development of infection it is not enough simply for bacteria to enter unnatural places of their existence. For the introduction of anaerobic flora and the development of an infectious pathological process, the participation of additional factors is necessary, which include large blood loss, local tissue ischemia, shock, starvation, stress, overwork, etc. Concomitant diseases (diabetes mellitus, collagenosis, malignant tumors, etc.) play an important role. ), long-term use of hormones and cytostatics, primary and secondary immunodeficiencies due to HIV infection and other chronic infectious and autoimmune diseases.
One of the main factors in the development of anaerobic infections is a decrease in the partial pressure of oxygen in tissues, which occurs both as a result of general causes (shock, blood loss, etc.) and local tissue hypoxia in conditions of insufficient arterial blood flow (occlusive vascular diseases), the presence of large the number of shell-shocked, crushed, non-viable tissues.
Irrational and inadequate antibiotic therapy, aimed mainly at suppressing antagonistic aerobic flora, also contributes to the unhindered development of anaerobes.
Anaerobic bacteria have a number of properties that allow them to exhibit their pathogenicity only when favorable conditions arise. Endogenous infections occur when the natural balance between the body's immune defense and virulent microorganisms is disrupted. Exogenous anaerobic infection, and especially clostridial infection, is more pathogenic and clinically more severe than infection caused by non-spore-forming bacteria.
Anaerobes have pathogenicity factors that contribute to their invasion into tissues, reproduction and the manifestation of pathogenic properties. These include enzymes, waste products and breakdown of bacteria, cell wall antigens, etc.
Thus, bacteroids, which mainly live in various parts of the gastrointestinal tract, upper respiratory tract and lower genitourinary tract, are capable of producing factors that promote their adhesion to the endothelium and damage it. Severe disorders of microcirculation are accompanied by increased vascular permeability, sludge of erythrocytes, microthrombosis with the development of immune complex vasculitis, which determines the progressive course of the inflammatory process and its generalization. Heparinase of anaerobes contributes to the occurrence of vasculitis, micro- and macrothrombophlebitis. The capsule of anaerobes is a factor that sharply increases their virulence, and even puts them in first place in associations. The secretion of neuraminidase, hyaluronidase, fibrinolysin, and superoxide dismutase by bacteroids due to their cytotoxic effect leads to tissue destruction and the spread of infection.
Bacteria of the genus Prevotella produce endotoxin, the activity of which exceeds the effect of lipopolysaccharides of bacteroids, and also produce phospholipase A, which disrupts the integrity of the membranes of epithelial cells, which leads to their death.
The pathogenesis of lesions caused by bacteria of the genus Fusobacterium is due to the ability to secrete leukocidin and phospholipase A, which exhibit a cytotoxic effect and facilitate invasion.
Gram-positive anaerobic cocci normally inhabit the oral cavity, colon, upper respiratory tract, and vagina. Their virulent and pathogenic properties have not been sufficiently studied, despite the fact that they are often detected during the development of very severe purulent-necrotic processes of various localizations. It is possible that the pathogenicity of anaerobic cocci is due to the presence of a capsule, the action of lipopolysaccharides, hyaluronidase and collagenase.
Clostridia are capable of causing both exogenous and endogenous anaerobic infection.
Their natural habitat is soil and the large intestine of humans and animals. The main genus-forming characteristic of clostridia is sporulation, which determines their resistance to unfavorable environmental factors.
In C. perfringens, the most common pathogenic microorganism, at least 12 toxin-enzymes and an enterotoxin have been identified, which determine its pathogenic properties:
- alpha-Toxin (lecithinase) - exhibits dermatonecrotizing, hemolytic and lethal effects.
- beta-Toxin - causes tissue necrosis and has a lethal effect.
- Sigma Toxin - exhibits hemolytic activity.
- theta-Toxin - has a dermatonecrotic, hemolytic and lethal effect.
- e-Toxins - cause lethal and dermatonecrotizing effects.
- c-Toxin (collagenase and gelatinase) - destroys reticular muscle tissue and connective tissue collagen fibers, has a necrotizing and lethal effect.
- lambda-Toxin (proteinase) - breaks down denatured collagen and gelatin, like fibrinolysin, causing necrotic properties.
- Gamma and Nu Toxins - have a lethal effect on laboratory animals.
- mu- and v-toxins (hyaluronidase and deoxyribon-clease) - increase tissue permeability.
Anaerobic infection is extremely rare and occurs as a monoinfection (less than 1% of cases). Anaerobic pathogens exhibit their pathogenicity in association with other bacteria. The symbiosis of anaerobes with each other, as well as with some types of facultative anaerobes, especially with streptococci, bacteria of the Enterobacteriaceae family, and non-fermenting gram-negative bacteria, makes it possible to create synergistic associative connections that facilitate their invasion and the manifestation of pathogenic properties.
How does anaerobic soft tissue infection manifest?
Clinical manifestations of anaerobic infections involving anaerobes are determined by the ecology of the pathogens, their metabolism, pathogenicity factors, which are realized in conditions of a decrease in the general or local immunoprotective forces of the macroorganism.
Anaerobic infection, regardless of the location of the outbreak, has a number of very characteristic clinical signs. These include:
- erasure of local classical signs of infection with a predominance of symptoms of general intoxication;
- localization of the source of infection in the usual habitat of anaerobes;
- unpleasant putrid odor of exudate, resulting from anaerobic oxidation of proteins;
- the predominance of processes of alterative inflammation over exudative inflammation with the development of tissue necrosis;
- gas formation with the development of emphysema and crepitus of soft tissues due to the formation of poorly soluble products of anaerobic metabolism of bacteria in water (hydrogen, nitrogen, methane, etc.);
- serous-hemorrhagic, purulent-hemorrhagic and purulent exudate with a brown, gray-brown color of the discharge and the presence of small droplets of fat in it;
- painting wounds and cavities black;
- development of infection due to long-term use of aminoglycosides.
If a patient has two or more of the signs described above, the likelihood of an anaerobic infection participating in the pathological process is very high.
Purulent-necrotic processes occurring with the participation of anaerobes can be divided into three clinical groups:
- The purulent process is local in nature, occurs without significant intoxication, quickly stops after surgical treatment or even without it, patients usually do not need intensive additional therapy.
- The clinical course of the infectious process is practically no different from ordinary purulent processes; it proceeds favorably, like an ordinary phlegmon with moderate symptoms of intoxication.
- The purulent-necrotic process proceeds violently, often malignantly; progresses, occupying large areas of soft tissue; Severe sepsis and MODS quickly develop with an unfavorable prognosis of the disease.
Anaerobic infection of soft tissues is characterized by heterogeneity and diversity, both in the severity of the pathological processes they cause, and in the pathomorphological changes that develop in the tissues with their participation. Various anaerobes, as well as aerobic bacteria, can cause the same type of diseases. At the same time, the same bacteria under different conditions can cause different diseases. However, despite this, several main clinical and pathomorphological forms of infectious processes involving anaerobes can be identified.
Various types of anaerobes can cause both superficial and deep purulent-necrotic processes with the development of serous and necrotic cellulitis, fasciitis, myositis and myonecrosis, combined lesions of several structures of soft tissues and bones.
Clostridial anaerobic infection is characterized by pronounced aggressiveness. In most cases, the disease is severe and rapid, with the rapid development of sepsis. Clostridial anaerobic infection develops in patients with various types of injuries to soft tissues and bones in the presence of certain conditions, which include massive soil contamination of the tissues, the presence in the wound of areas of dead and crushed tissue deprived of blood supply, and the presence of foreign bodies. Endogenous clostridial anaerobic infection occurs in acute paraproctitis, after operations on the abdominal organs and lower extremities in patients with obliterating vascular diseases and diabetes mellitus. Less common is an anaerobic infection that develops as a result of a human or animal bite or injection of drugs.
Clostridial anaerobic infection occurs in two main pathomorphological forms: cellulitis and myonecrosis.
Clostridial cellulitis (crepitating cellulitis) is characterized by the development of necrosis of subcutaneous or intermuscular tissue in the wound area. It is proceeding relatively favorably. Wide, timely dissection of the wound and excision of non-viable tissue in most cases ensures recovery.
In patients with diabetes mellitus and obliterating diseases of the vessels of the lower extremities, there is less chance of a favorable outcome of the disease, since the infectious process in the form of cellulite occurs only in the first stages, then purulent-necrotic tissue damage quickly moves to deeper structures (tendons, muscles, bones). A secondary gram-negative anaerobic infection is associated with the involvement of the entire complex of soft tissues, joints and bone structures in the purulent-necrotic process. Wet gangrene of the limb or its segment is formed, and therefore it is often necessary to resort to amputation.
Clostridial myonecrosis (gas gangrene) is the most severe form of anaerobic infection. The duration of the incubation period ranges from several hours to 3-4 days. Severe, bursting pain in the wound occurs, which is the earliest local symptom. The condition remains without visible changes. Later, progressive swelling appears. The wound becomes dry, and a foul-smelling discharge with gas bubbles appears. The skin takes on a bronze color. Intradermal blisters with serous-hemorrhagic exudate and foci of wet skin necrosis of a purplish-cyanotic and brown color quickly form. Gas formation in tissues is a common sign of anaerobic infection.
In parallel with local symptoms, the general condition of the patient worsens. Against the background of massive endotoxicosis, the processes of dysfunction of all organs and systems are rapidly increasing with the development of severe anaerobic sepsis and septic shock, from which patients die if surgical care is not provided in full on time.
A characteristic sign of infection is muscle damage by necrotic process. They become flabby, dull, bleed poorly, do not contract, acquire a dirty brown color and have the consistency of “boiled meat.” As the process progresses, anaerobic infection quickly spreads to other muscle groups and neighboring tissues with the development of gas gangrene.
A rare cause of clostridial myonecrosis is injection of medicinal drugs. Treatment of such patients is challenging. Only a few patients' lives can be saved. The case history below illustrates one such case.
Anaerobic streptococcal cellulitis and myositis occur as a result of various soft tissue injuries, surgical operations and manipulations. They are caused by gram-positive facultative anaerobes Streptococcus spp. and anaerobic cocci (Peptostreptococcus spp., Peptococcus spp.). The disease is characterized by the development in the early stages of predominantly serous, and in the later stages of necrotic cellulitis or myositis and occurs with symptoms of severe intoxication, often turning into septic shock. Local symptoms of infection are erased. Tissue edema and hyperemia are not expressed, fluctuation is not determined. Gas formation occurs rarely. With necrotic cellulite, the fiber looks faded, bleeds poorly, is gray in color, and is abundantly saturated with serous and serous-purulent exudate. The skin is involved in the inflammatory process for the second time: cyanotic spots with uneven edges and blisters with serous contents appear. The affected muscles look swollen, contract poorly, and are saturated with serous, serous-purulent exudate.
Due to the paucity of local clinical signs and the prevalence of symptoms of severe endotoxicosis, surgical intervention is often performed late. Timely surgical treatment of the inflammatory focus with intensive antibacterial and detoxification therapy quickly interrupts the course of anaerobic streptococcal cellulitis or myositis.
Synergistic necrotizing cellulitis is a severe, rapidly progressive purulent-necrotic disease of the tissue caused by an associative non-clostridial anaerobic infection and aerobes. The disease occurs with uncontrollable destruction of fiber and secondary involvement of neighboring tissues (skin, fascia, muscles) in the purulent-necrotic process. The skin is most often involved in the pathological process. Purple-cyanotic confluent spots appear without a clear boundary, later turning into wet necrosis with ulcerations. As the disease progresses, vast areas of various tissues, primarily muscles, are involved in the infectious process, and non-clostridial gangrene develops.
Necrotizing fasciitis is a synergistic anaerobic-aerobic, rapidly progressive purulent-necrotic process with damage to the superficial fascia of the body. In addition to anaerobic non-clostridial infection, the causative agents of the disease are often streptococci, staphylococci, enterobacteria and Pseudomonas aeruginosa, which are usually determined in association with each other. In most cases, the underlying areas of fiber, skin, and superficial layers of muscles are secondarily involved in the inflammatory process. Necrotizing fasciitis usually develops after soft tissue trauma and surgery. Minimal external signs of infection usually do not correspond to the severity of the patient’s condition and the massive and widespread tissue destruction that is detected intraoperatively. Delayed diagnosis and late surgical intervention often lead to a fatal outcome of the disease.
Fournier syndrome (Fournier J., 1984) is one of the types of anaerobic infection. It is manifested by progressive necrosis of the skin and underlying tissues of the scrotum with rapid involvement in the process of the skin of the perineum, pubis, and penis. Wet anaerobic gangrene of the perineal tissue (Fournier's gangrene) often forms. The disease develops spontaneously or as a result of minor trauma, acute paraproctitis or other purulent diseases of the perineum and occurs with severe symptoms of toxemia and septic shock. Often it ends in the death of patients.
In a real clinical situation, especially in the later stages of the infectious process, it can be quite difficult to distinguish between the above-described clinical and morphological forms of diseases caused by anaerobes and their associations. Often, during surgery, damage to several anatomical structures is detected at once in the form of necrotizing fasciocellulitis or fasciomyositis. Often the progressive nature of the disease leads to the development of non-clostridial gangrene with the involvement of the entire thickness of soft tissue in the infectious process.
The purulent-necrotic process caused by anaerobes can spread to soft tissues from the internal organs of the abdominal and pleural cavities affected by the same infection. One of the factors predisposing to this is inadequate drainage of a deep purulent focus, for example, with pleural empyema and peritonitis, in the development of which anaerobes are involved in almost 100% of cases.
Anaerobic infection is characterized by a violent onset. The symptoms of severe endotoxemia (high fever, chills, tachycardia, tachypnea, lack of appetite, lethargy, etc.) usually come to the fore, which often precede the development of local signs of the disease by 1-2 days. In this case, some of the classic symptoms of purulent inflammation (swelling, hyperemia, pain, etc.) disappear or remain hidden, which complicates timely pre-hospital, and sometimes in-hospital, diagnosis of anaerobic phlegmon and delays the start of surgical treatment. It is characteristic that patients themselves often do not associate their “disease” with the local inflammatory process until a certain time.
In a significant number of observations, especially with anaerobic necrotizing fasciocellulitis or myositis, when local symptoms are dominated by only moderate hyperemia or tissue swelling in the absence of fluctuation, the disease occurs under the guise of another pathology. These patients are often hospitalized with a diagnosis of erysipelas, thrombophlebitis, lymphovenous insufficiency, ileofemoral thrombosis, deep vein thrombosis of the leg, pneumonia, etc., and sometimes in non-surgical hospital departments. Late diagnosis of severe soft tissue infection is fatal for many patients.
How is anaerobic infection recognized?
Anaerobic soft tissue infection is differentiated from the following diseases:
- purulent-necrotic lesions of soft tissues of other infectious etiology;
- various forms of erysipelas (erythematous-bulous, bullous-hemorrhagic);
- soft tissue hematomas with symptoms of intoxication;
- blistering dermatoses, severe toxic derma (polymorphic exudative erythema, Steven-Johnson syndrome, Lyell's syndrome, etc.);
- deep vein thrombosis of the lower extremities, ileofemoral thrombosis, Paget-Schroetter syndrome (thrombosis of the subclavian vein);
- syndrome of prolonged tissue crushing in the early stages of the disease (at the stage of purulent complications, the addition of an anaerobic infection is usually determined);
- frostbite of II-IV degree;
- gangrenous-ischemic changes in soft tissues against the background of acute and chronic thrombobliterating diseases of the arteries of the extremities.
Infectious emphysema of soft tissues, which develops as a result of the activity of anaerobes, must be differentiated from emphysema of other etiologies associated with pneumothorax, pneumoperitoneum, perforation of hollow abdominal organs into the retroperitoneal tissue, surgical interventions, washing wounds and cavities with a solution of hydrogen peroxide, etc. In addition to crepitus soft tissues usually lack local and general signs of anaerobic infection.
The intensity of the spread of the purulent-necrotic process during anaerobic infection depends on the nature of the interaction between the macro- and microorganism, on the ability of the immune defense to resist factors of bacterial aggression. Fulminant anaerobic infection is characterized by the fact that already within the first day a widespread pathological process develops, affecting tissue over a large area and accompanied by the development of severe sepsis, uncorrectable MODS and septic shock. This malignant variant of the infection leads to the death of more than 90% of patients. In the acute form of the disease, such disturbances in the body develop within several days. Subacute anaerobic infection is characterized by the fact that the relationship between macro- and microorganisms is more balanced, and with timely initiation of complex surgical treatment, the disease has a more favorable outcome.
Microbiological diagnosis of anaerobic infection is extremely important not only due to scientific interest, but also necessary for practical needs. Until now, the clinical picture of the disease has been the main method for diagnosing anaerobic infection. However, only microbiological diagnostics with identification of the causative agent of infection can certainly give an answer about the participation of anaerobes in the pathological process. Meanwhile, a negative response from the bacteriological laboratory in no way rejects the possibility of the participation of anaerobes in the development of the disease, since according to some data, about 50% of anaerobes are uncultivable.
Anaerobic infection is diagnosed using modern high-precision indication methods. These primarily include gas-liquid chromatography (GLC) and mass spectrometry, based on the registration and quantification of metabolites and volatile fatty acids. The data from these methods correlate with the results of bacteriological diagnostics in 72%. The sensitivity of GLC is 91-97%, specificity is 60-85%.
Other promising methods for isolating anaerobic pathogens, including from blood, include the Lachema, Bactec, Isolator systems, staining preparations for detecting bacteria or their antigens in the blood with acridine yellow, immunoelectrophoresis, enzyme-linked immunosorbent assay and others.
An important task of clinical bacteriology at the present stage is to expand research into the species composition of pathogens with the identification of all species involved in the development of the wound process, including anaerobic infection.
It is believed that most infections of soft tissues and bones are of a mixed, polymicrobial nature. According to V.P. Yakovlev (1995), with extensive purulent diseases of soft tissues, obligate anaerobes are found in 50% of cases, in combination with aerobic bacteria in 48%, in monoculture anaerobes are detected only in 1.3%.
However, it seems difficult in practice to determine the true ratio of species composition with the participation of facultative anaerobic, aerobic and anaerobic microorganisms. This is largely due to the difficulty of identifying anaerobic bacteria due to some objective and subjective reasons. The first includes the fastidiousness of anaerobic bacteria, their slow growth, the need for special equipment, highly nutritious media with specific additives for their cultivation, etc. The second includes significant financial and time costs, the need for strict implementation of protocols for multi-stage and repeated studies, and a shortage of qualified specialists.
However, in addition to academic interest, the identification of anaerobic microflora is of great clinical importance both in determining the etiology of the primary purulent-necrotic lesion and sepsis, and in developing therapeutic tactics, including antibiotic therapy.
Below are demonstrated standard schemes for studying the microflora of a purulent focus and blood in the presence of clinical signs of anaerobic infection, used in the bacteriological laboratory of our clinic.
Each study begins with a Gram stain of an imprint smear from the deep tissues of a purulent focus. This study is one of the methods for rapid diagnosis of wound infections and can, within one hour, give an approximate answer about the nature of the microflora present in the purulent focus.
It is imperative to use means to protect microorganisms from the toxic effects of oxygen, for which they use:
- microanaerostat for cultivating crops;
- commercial gas generator packages (GasPak or HiMedia) to create anaerobiosis conditions;
- anaerobiosis indicator: inoculation of P. aeruginosa on Simons citrate under anaerobic conditions (P. aeruginosa does not utilize citrate, and the color of the medium does not change).
Immediately after the operation, smears and biopsies from the deep parts of the wound taken from one locus are delivered to the laboratory. To deliver samples, special transport systems of several types are used.
If bacteremia is suspected, blood is inoculated in parallel into 2 vials (10 ml each) with commercial media for testing for aerobic and anaerobic microorganisms.
Sowing is carried out using disposable plastic loops for several media:
- onto freshly poured Schedler's blood agar with the addition of vitamin K + hemin complex - for cultivation in a microanaerostat. During primary sowing, a disk with kanamycin is used to create selective conditions (most anaerobes are naturally resistant to aminoglycosides);
- 5% blood agar for cultivation under aerobic conditions;
- to an enrichment medium for cultivation in a microanaerostat (increases the likelihood of pathogen release, thioglycollate or iron sulfite if a clostridial infection is suspected.
A microanaerostat and a plate with 5% blood agar are placed in a thermostat and incubated at +37 C for 48-72 hours. Smears delivered on glass slides are stained with Gram. It is advisable to take several smears of wound fluid during surgery.
Already with microscopy, in some cases it is possible to make a presumptive conclusion about the nature of the infection, since certain types of anaerobic microorganisms have a characteristic morphology.
Obtaining a pure culture confirms the diagnosis of clostridial infection.
After 48-72 hours of incubation, colonies grown under aerobic and anaerobic conditions are compared according to their morphology and microscopy results.
Colonies grown on Schedler agar are tested for aerotolerance (several colonies of each type). They are seeded in parallel sectors onto two plates: with Schedler agar and 5% blood agar.
Colonies grown in the corresponding sectors under aerobic and anaerobic conditions are considered indifferent to oxygen and are examined according to existing methods for facultative anaerobic bacteria.
Colonies grown only under anaerobic conditions are regarded as obligate anaerobes and are identified taking into account:
- morphology and size of colonies;
- presence or absence of hemolysis;
- presence of pigment;
- ingrowth into agar;
- catalase activity;
- generic sensitivity to antibiotics;
- cell morphology;
- biochemical characteristics of the strain.
The identification of microorganisms is greatly facilitated by the use of commercial test systems containing more than 20 biochemical tests that make it possible to determine not only the genus, but also the type of microorganism.
Micropreparations of some types of anaerobes isolated in pure culture are presented below.
Detection and identification of an anaerobic pathogen from the blood is possible in rare cases, such as, for example, a culture of P. niger isolated from the blood of a patient with a picture of severe wound anaerobic sepsis against the background of thigh phlegmon.
Sometimes associations of microorganisms may contain contaminants that do not have an independent etiological role in the infectious-inflammatory process. Isolation of such bacteria in monoculture or in association with pathogenic microorganisms, especially when analyzing biopsies from deep wounds, may indicate low nonspecific resistance of the organism and, as a rule, is associated with a poor prognosis of the disease. Similar results of bacteriological examination are not uncommon in severely weakened patients, in patients with diabetes mellitus, with immunodeficiency states against the background of various acute and chronic diseases.
In the presence of a purulent focus in soft tissues, bones or joints and a clinical picture of an anaerobic infection (clostridial or non-clostridial), the overall frequency of anaerobic isolation, according to our data, is 32%. The frequency of detection of obligate anaerobes in the blood in these diseases is 3.5%.
How is an anaerobic infection treated?
Anaerobic infection is mainly treated by surgical intervention and complex intensive care. Surgical treatment is based on radical COGO, followed by repeated treatment of an extensive wound and its closure using available plastic methods.
The time factor in organizing surgical care plays an important, sometimes decisive role. A delay in surgery leads to the spread of infection over large areas, worsening the patient's condition and increasing the risk of the intervention itself. The steadily progressive nature of the course of anaerobic infection is an indication for emergency or urgent surgical treatment, which should be performed after short-term preliminary preoperative preparation, which consists in eliminating hypovolemia and gross disturbances of homeostasis. In patients with septic shock, surgical intervention is possible only after stabilization of blood pressure and resolution of oligoanuria.
Clinical practice has shown that it is necessary to abandon the so-called “lamps” incisions without necrectomy, which were widely accepted several decades ago and have not yet been forgotten by some surgeons. Such tactics lead to the death of patients in almost 100% of cases.
During surgical treatment, it is necessary to perform a wide dissection of tissues affected by infection, with incisions extending to the level of visually unaltered areas. The spread of anaerobic infection is characterized by pronounced aggressiveness, overcoming various barriers in the form of fascia, aponeuroses and other structures, which is not typical for infections that occur without the dominant participation of anaerobes. Pathomorphological changes in the focus of infection can be extremely heterogeneous: areas of serous inflammation alternate with areas of superficial or deep tissue necrosis. The latter can be located at considerable distances from each other. In some cases, the maximum pathological changes in tissues are detected far from the entrance gates of the infection.
In connection with the noted features of spread in anaerobic infections, a thorough inspection of the source of inflammation should be carried out with extensive mobilization of skin-fat and skin-fascial flaps, dissection of fascia and aponeuroses with revision of intermuscular, paravasal, paraneural tissue, muscle groups and each muscle separately. Insufficient revision of the wound leads to an underestimation of the prevalence of phlegmon, the volume and depth of tissue damage, which leads to insufficiently complete CHO and the inevitable progression of the disease with the development of sepsis.
With COGO, it is necessary to remove all non-viable tissue, regardless of the extent of the lesion. Skin patches of pale cyanotic or purple color are already deprived of blood supply due to vascular thrombosis. They must be removed en bloc with the underlying fatty tissue. All affected areas of fascia, aponeuroses, muscles and intermuscular tissue are also subject to excision. In areas adjacent to serous cavities, large vascular and nerve trunks, and joints, certain restraint must be exercised during necrectomy.
After radical HOGO, the edges and bottom of the wound should be visually unchanged tissue. The area of the wound after surgery can occupy from 5 to 40% of the body surface. There is no need to be afraid of the formation of very large wound surfaces, since complete necrectomy is the only way out to save the patient’s life. Palliative surgical treatment inevitably leads to the progression of phlegmon, systemic inflammatory response syndrome and a worsening prognosis of the disease.
For anaerobic streptococcal cellulitis and myositis in the stage of serous inflammation, surgical intervention should be more restrained. Wide spreading of skin-fat flaps, circular exposure of a group of affected muscles with spreading of intermuscular tissue is sufficient to stop the process with adequate intensive detoxification and targeted antibacterial therapy. For necrotizing cellulite and myositis, surgical tactics are similar to those described above.
In case of clostridial myositis, depending on the volume of the lesion, a muscle, a group or several muscle groups, non-viable areas of skin, subcutaneous fat and fascia are removed.
If, during revision of the surgical wound, a significant amount of tissue damage (gangrene or the possibility of the latter) is revealed with insignificant prospects for preserving the functional ability of the limb, then amputation or disarticulation of the limb is indicated in this situation. Radical intervention in the form of limb truncation should also be resorted to in patients with extensive tissue damage to one or several segments of the limb in cases of severe sepsis and uncorrectable MODS, when the prospect of saving the limb is fraught with the loss of the patient’s life, as well as in cases of fulminant anaerobic infection.
Limb amputation due to anaerobic infection has its own characteristics. It is performed in a circular manner, without the formation of musculocutaneous flaps, within healthy tissues. To obtain a longer limb stump, A.P. Kolesov et al. (1989) propose to perform amputation at the border of the pathological process with dissection and separation of the soft tissues of the stump. In all cases, the stump wound is not sutured; it is treated openly with loose tamponade using water-soluble ointments or iodophor solutions. The group of patients who have had a limb amputated is the most severe. Postoperative mortality, despite complex intensive therapy, remains high - 52%.
Anaerobic infection is characterized by the fact that the inflammation is prolonged in nature with a slowdown in the change of phases of the wound process. The phase of cleansing the wound from necrosis is sharply delayed. The development of granulations is delayed due to the polymorphism of the processes occurring in the soft tissues, which is associated with gross microcirculatory disorders and secondary infection of the wound. This is also associated with the need for repeated surgical treatment of a purulent-necrotic focus (Fig. 3.66.1), during which secondary necrosis is removed, new purulent leaks and pockets are opened, and the wound is thoroughly sanitation using additional methods of influence (ultrasonic cavitation, treatment with a pulsating jet antiseptics, ozonation, etc.). Progression of the process with the spread of anaerobic infection to new areas serves as an indication for emergency repeated COGO. Refusal from staged necrectomy is possible only after persistent relief of the local purulent-inflammatory process and SIRS phenomena.
The immediate postoperative period in patients with severe anaerobic infection takes place in the intensive care unit, where intensive detoxification therapy, antibiotic therapy, treatment of multiple organ dysfunction, adequate pain relief, parenteral and enteral tube nutrition, etc. are carried out. The indications for transferring the patient to the surgical department of the hospital are positive dynamics during the wound process, completion of the stage of repeated surgical treatment of the purulent focus, and sometimes plastic interventions, persistent clinical and laboratory elimination of MOF phenomena.
Antibiotic therapy is an important link in the treatment of patients with a disease such as anaerobic infection. Considering the mixed microbial etiology of the primary purulent-necrotic process, first of all, broad-spectrum drugs are prescribed, including antianaerobic drugs. The most commonly used combinations of drugs are: II-IV generation cephalosporins or fluoroquinolones in combination with metronidazole, dioxidine or clindamycin, carbapenems in monotherapy.
Monitoring the dynamics of the course of the wound process and sepsis, microbiological monitoring of discharge from wounds and other biological media allow timely adjustments to be made in changing the composition, dosage and methods of administration of antibiotics. Thus, during the treatment of severe sepsis against the background of an anaerobic infection, antibacterial therapy regimens can change from 2 to 8 or more times. Indications for its cancellation are persistent relief of inflammatory phenomena in the primary and secondary purulent foci, healing of the wound after plastic surgery, negative results of blood cultures and absence of fever for several days.
An important component of complex surgical treatment of patients with anaerobic infection is local wound treatment.
The use of one or another dressing is planned depending on the stage of the wound process, pathomorphological changes in the wound, the type of microflora, as well as its sensitivity to antibiotics and antiseptics.
In the first phase of the wound process in the case of anaerobic or mixed infection, the drugs of choice are ointments on a hydrophilic basis with an antianaerobic effect - dioxicol, streptonitol, nitacid, iodopyronic, 5% dioxidine ointments, etc. If there is gram-negative flora in the wound, they are used as ointments on a hydrophilic basis, and antiseptics - 1% solutions of iodophors, 1% solution of dioxidine, solutions of miramistin, sodium hypochlorite, etc.
In recent years, we have widely used modern application-sorption therapy of wounds with biologically active swelling sorbents of multicomponent action on the wound process such as lysosorb, colladia-sorb, diotevin, anilodyotevin, etc. These agents cause a pronounced anti-inflammatory, hemostatic, anti-edematous, antimicrobial effect on almost all types of wounds. bacterial flora, allow for necrolysis, transform wound discharge into a gel, absorb and remove toxins, decay products and microbial bodies outside the wound. The use of biologically active drainage sorbents makes it possible to stop the purulent-necrotic process and inflammatory phenomena in the wound area in the early stages and prepare it for plastic closure.
The formation of extensive wound surfaces resulting from surgical treatment of a widespread purulent focus creates the problem of their rapid closure with various types of plastic surgery. Plastic surgery must be performed as early as possible, as far as the condition of the wound and the patient allows. In practice, plastic surgery can be carried out no earlier than the end of the second - beginning of the third week, which is associated with the above-described features of the course of the wound process during anaerobic infection.
Early plastic surgery of a purulent wound is considered one of the most important elements of complex surgical treatment of anaerobic infection. The rapid elimination of extensive wound defects, through which massive loss of proteins and electrolytes occurs, the wound is contaminated with hospital polyantibiotic-resistant flora with tissue involvement in the secondary purulent-necrotic process, is a pathogenetically justified and necessary surgical measure aimed at treating sepsis and preventing its progression.
In the early stages of plastic surgery, it is necessary to use simple and least traumatic methods, which include plastic surgery with local tissues, dosed tissue stretching of tissues, ADP, and a combination of these methods. Complete (simultaneous) skin grafting can be performed in 77.6% of patients. In the remaining 22.4% of patients, the wound defect, due to the peculiarities of the course of the wound process and its extensiveness, can only be closed in stages.
Mortality in the group of patients who underwent a complex of plastic interventions was almost 3.5 times lower than in the group of patients who did not undergo plastic surgery or were performed at a later stage, 12.7% and 42.8%, respectively.
The overall postoperative mortality rate for severe anaerobic infection of soft tissues, with the prevalence of a purulent-necrotic focus over an area of more than 500 cm 2, is 26.7%.
Knowledge of the clinical features of the course allows the practical surgeon to identify such a life-threatening disease as an anaerobic infection in the early stages and plan a set of response diagnostic and therapeutic measures. Timely radical surgical treatment of an extensive purulent-necrotic lesion, repeated staged necrectomy, early skin grafting in combination with multicomponent intensive therapy and adequate antibacterial treatment can significantly reduce mortality and improve treatment results.
100. Anaerobic infection of soft tissues: etiology, classification, clinical picture, diagnosis, principles of treatment.
Modern advances in the treatment of anaerobic infection.
101. Anaerobic infection. Features of the flow. Principles of surgical treatment.
The variety of clinical manifestations of this infection is indicated by the abundance of names (up to 70) and classifications of clinical forms. They characterize certain manifestations that predominate in a given picture of the disease. For example, the pathological process is called anaerobic erysipelas; if the phenomena of hyperemia of the skin predominate, an anaerobic abscess, if cavities are formed with decay, ichorous-hemorrhagic fluid, sometimes with gases. There are epifascial, superficial, mild forms and subfascial, more severe forms. Classic signs of inflammation in these infections are mild or absent.
Regardless of the location of the outbreak, there are general and very characteristic clinical features of infectious processes occurring with the participation of anaerobes. Many clinical features of this type of infection are explained by the peculiarities of the metabolism of anaerobes, primarily by the putrefactive nature of the lesion and gas formation. The most constant symptom: the unpleasant, putrid smell of exudate is the result of anaerobic oxidation of the protein substrate. It was known at the end of the 19th century. but as a result of the shift in clinical microbiology toward the aerobic side over the years, this symptom began to be attributed to Escherichia coli. In fact, not all anaerobes form unpleasant-smelling substances, so the absence of this sign does not allow us to completely reject the presence of anaerobes. On the other hand, stench always indicates its anaerobic origin. The second feature of anaerobic damage is its putrefactive nature. The lesions contain dead tissue of a gray, gray-green color. The third is the color of the exudate - gray-green, brown. The color is heterogeneous and contains droplets of fat. The pus is liquid, often diffusely permeating the inflamed tissue. Whereas with aerobic suppuration, the pus is thick, the color is uniform, dark yellow, and there is no odor. It should be noted that the distinctive signs of certain infections appear more clearly in the early stages of the disease.
Local phenomena: pallor of the skin with clearly defined saphenous veins, sometimes blue spots or bronze stripes, swelling of the tissues, sometimes crepitus under the skin. Sharp pain at the very beginning of the development of the process, followed by a feeling of fullness and heaviness in the limb due to inflation with gas and an increase in volume as a result of swelling of the soft tissues. When gas appears in the tissues of the affected limb, upon palpation, a special sound occurs, similar to the sensation obtained when shaving hair (razor symptom). Sometimes blisters appear on the skin due to the fact that edematous fluid penetrates the epidermal layer and lifts it.
Clinically, the severity of anaerobic soft tissue infection largely depends on the volume of affected tissue. The infection can be predominantly localized in the subcutaneous tissue, fascia, muscles, or affect these structures simultaneously.
When subcutaneous tissue is affected, the skin over this area is usually little changed. There is dense swelling and hyperemia without clear delineation. A relatively small change in the skin does not reflect the true extent of damage to the underlying tissues. The pathological process can spread far beyond the boundaries of the primary focus. Fatty tissue appears as foci of fusion of a gray-dirty color, the exudate is brown, often with an unpleasant odor, freely flowing into the wound. The presence of dense infiltration of subcutaneous tissue and areas of darkening or necrosis of the skin due to thrombosis of small vessels indicates the transition of the process to the fascia. The presence in the wound of melted, gray-dirty areas of necrotically altered fascia and brown exudate allows us to consider the diagnosis of non-clostridial infection as undoubted. Combined damage to the subcutaneous tissue, fascia and muscles is possible. In this case, the process often extends far beyond the boundaries of the primary focus. The muscles are dull, boiled, soaked in serous-hemorrhagic exudate, disintegrate when touched, and bloodless.
Surgery and intensive care with targeted use of antibiotics are the basis of treatment for patients with anaerobic infection. Patients are advised to be examined by a resuscitator to determine the severity of the condition and the need for preoperative preparation. An established diagnosis of anaerobic infection serves as an indication for emergency surgery, which is performed immediately upon admission or after preoperative infusion preparation under the control of blood pressure, central venous pressure and diuresis.
Surgery for anaerobic wound infection is performed under general anesthesia.
Differentiated approach to the scope of surgical intervention: - In case of isolated damage to layers (skin, subcutaneous tissue, fascia, muscles) without a life-threatening condition - necrectomy. - In case of total tissue damage with a life-threatening condition - amputation of the limb.
In the presence of bone fractures, after necrectomy, extrafocal fixation of the fractures is advisable.
The mandatory scope of surgical intervention includes:- Dissection of soft tissues to verify the limits of healthy tissues - removal of non-viable tissues - subcutaneous tissue, fascia, muscles, loose bone fragments.
Incisions should also be made in cases accompanied only by tissue swelling, to reduce tissue tension and venous stagnation, improve blood circulation, due to which the body is freed from a large number of toxins. Amputation is performed without a tourniquet, using a circular incision with the intersection of all tissues at the same level within healthy tissue, without treating the nerve and without sutures to the muscles and skin. Disarticulation is indicated for highly prevalent processes and severe intoxication, but it has a high mortality rate.
With the traditional “clostridial” understanding of anaerobic infection, stripe incisions are often used as an operative aid. This method has a limited right to exist and is of purely auxiliary value. In principle, the surgeon should strive for radical treatment of the lesion, which consists, if possible, in obtaining a clean wound.
For non-clostridial soft tissue infection, the operation consists of radical debridement of the wound with excision of all non-viable tissue. During surgery, it is necessary to make a wide dissection of the skin, starting from the border of its changed color, as well as the tissues of the entire affected area with complete removal of the pathologically changed subcutaneous tissue, fascia, and muscle without fear of the appearance of an extensive wound surface. It is important to stop the progression of the infection and save the patient’s life. Skin flaps along the edges of the surgical wound must be spread wide, placed on sterile gauze rolls and sutured with separate sutures to nearby areas of unaffected skin. This provides the best wound aeration and visual control of the wound process. With this type of wound management in the postoperative period, it is easy to detect areas of affected tissue, which is the result of non-radical intervention or a sign of disease progression. The only way to save the patient’s life is radical excision of all affected tissues, and one should not be afraid of the formation of extensive wound surfaces after the operation. If the limbs are affected, it is necessary to raise the question of amputation. For large, deep wounds with numbness, it is recommended to use loose wound tamponade with hydrogen peroxide wipes. The use of potassium permanganate immediately after surgery should be limited, despite its high antianaerobic activity. This is due to the ability of the drug to stain tissue, mainly subcutaneous tissue, which can cause difficulties in assessing the condition of tissue (development of necrosis) during subsequent revision. The first dressing is performed a day later, always under anesthesia. If necrotic tissue is detected, they are excised. Observe the wound for 3-4 days. Subsequently, if the general condition is positive and there are no signs of the process spreading beyond the wound, the skin sutures are removed, the wound is loosely packed with antiseptic wipes, and skin flaps are placed on the wound. When the process stabilizes, a transition to osmotically active ointments is possible. Observe local changes in the wound under conditions of reduced aeration for 1-2 days. Subsequently, early secondary sutures are applied and flow-aspiration drainage is performed. The drains are removed approximately after 3-5 days under the control of the general condition of the patient, the nature and amount of discharge through the drains. In the absence of a secondary infection, mainly Pseudomonas aeruginosa, these wounds, as a rule, heal by primary intention. In some cases, autodermoplasty with a free mesh flap can be performed.
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Once a child is diagnosed with diabetes, parents often go to the library for information on the subject and are faced with the possibility of complications. After a period of worry, parents are hit with the next blow when they learn about diabetes-related morbidity and mortality statistics.
Viral hepatitis in early childhood
Relatively recently, the hepatitis alphabet, which already included hepatitis viruses A, B, C, D, E, G, was replenished with two new DNA-containing viruses, TT and SEN. We know that hepatitis A and hepatitis E do not cause chronic hepatitis and that hepatitis G and TT viruses are most likely “innocent spectators” that are transmitted vertically and do not affect the liver.
Measures for the treatment of chronic functional constipation in children
When treating chronic functional constipation in children, it is necessary to take into account important factors in the child's medical history; establish a good relationship between the health care professional and the child-family to ensure that the proposed treatment is carried out properly; a lot of patience on both sides, with repeated assurances that the situation will gradually improve, and courage in cases of possible relapses, constitute the best way to treat children suffering from constipation.
Scientists' study findings challenge assumptions about diabetes treatment
The results of a ten-year study have indisputably proven that frequent self-monitoring and maintaining blood glucose levels within normal limits leads to a significant reduction in the risk of late complications caused by diabetes and a decrease in their severity.
Manifestations of rickets in children with impaired formation of the hip joints
In the practice of pediatric orthopedists and traumatologists, the question is often raised about the need to confirm or exclude disorders of the formation of the hip joints (hip dysplasia, congenital hip dislocation) in infants. The article shows an analysis of a survey of 448 children with clinical signs of disorders of the formation of the hip joints.
Medical gloves as a means of ensuring infection safety
Most nurses and doctors don't like gloves, and for good reason. Wearing gloves, the sensitivity of your fingertips is lost, the skin on your hands becomes dry and flaky, and the instrument tends to slip out of your hands. But gloves have been and remain the most reliable means of protection against infection.
Lumbar osteochondrosis
It is believed that every fifth adult on earth suffers from lumbar osteochondrosis; this disease occurs in both young and old age.
Epidemiological control over health workers who had contact with the blood of HIV-infected people
(to help medical workers in medical institutions)
The guidelines cover the issues of monitoring medical workers who have had contact with the blood of a patient infected with HIV. Actions are proposed to prevent occupational HIV infection. A logbook and an official investigation report for contact with the blood of an HIV-infected patient have been developed. The procedure for informing higher authorities about the results of medical observation of health workers who came into contact with the blood of an HIV-infected patient has been determined. Intended for medical workers of treatment and preventive institutions.
Chlamydial infection in obstetrics and gynecology
Chlamydia of the genitals is the most common sexually transmitted disease. All over the world, there is an increase in chlamydia among young women who have just entered the period of sexual activity.
Cycloferon in the treatment of infectious diseases
Currently, there is an increase in certain nosological forms of infectious diseases, primarily viral infections. One of the directions for improving treatment methods is the use of interferons, as important nonspecific factors of antiviral resistance. These include cycloferon, a low molecular weight synthetic inducer of endogenous interferon.
Dysbacteriosis in children
The number of microbial cells present on the skin and mucous membranes of a macroorganism in contact with the external environment exceeds the number of cells of all its organs and tissues combined. The weight of the microflora of the human body is on average 2.5-3 kg. The importance of microbial flora for a healthy person was first noticed in 1914 by I.I. Mechnikov, who suggested that the cause of many diseases are various metabolites and toxins produced by various microorganisms that inhabit the organs and systems of the human body. The problem of dysbacteriosis in recent years has caused a lot of discussions with an extreme range of opinions.
Diagnosis and treatment of infections of the female genital organs
In recent years, throughout the world and in our country, there has been an increase in the incidence of sexually transmitted infections among the adult population and, which is of particular concern, among children and adolescents. The incidence of chlamydia and trichomoniasis is increasing. According to WHO, trichomoniasis ranks first in frequency among sexually transmitted infections. Every year, 170 million people worldwide become ill with trichomoniasis.
Intestinal dysbiosis in children
Intestinal dysbiosis and secondary immunodeficiency are increasingly encountered in the clinical practice of doctors of all specialties. This is due to changing living conditions and the harmful effects of the preformed environment on the human body.
Viral hepatitis in children
The lecture “Viral hepatitis in children” presents data on viral hepatitis A, B, C, D, E, F, G in children. All clinical forms of viral hepatitis, differential diagnosis, treatment and prevention that currently exist are presented. The material is presented from a modern perspective and is intended for senior students of all faculties of medical universities, interns, pediatricians, infectious disease specialists and doctors of other specialties who are interested in this infection.
Prevention of tetanus. Emergency prevention of tetanus involves not only primary surgical treatment of the wound with the removal of foreign bodies and necrotic tissue, 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, out-of-hospital abortions and childbirth, gangrene and tissue necrosis, 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 mainly for emergency immunization.
Vaccination regimen: the 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.
Adsorbed diphtheria-tetanus toxoid with reduced antigen content (ADS-M toxoid) is a vaccine for the prevention of diphtheria and tetanus with reduced antigen content. Intended 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 after achieving complete or partial remission, people with neurological diseases are vaccinated after the progression of the process has been excluded, patients with allergic diseases are vaccinated 2-4 weeks after the end of the exacerbation.
Equine anti-tetanus serum purified concentrated liquid (PSS) - contains antitoxins that neutralize tetanus toxin. Used for treatment and emergency specific prevention of tetanus
Compound: 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 the drugs, each vaccinated person must be under medical supervision for an hour after vaccination. If symptoms of shock appear, immediate anti-shock therapy is necessary. Persons who have received PSS should be warned about the need to immediately seek medical help in case of fever, itching and rashes on the skin, joint pain and other symptoms characteristic of serum sickness.
Anti-tetanus human immunoglobulin (ATHI) 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 temperatures below 0°C. Intended for emergency prophylaxis of tetanus instead of equine anti-tetanus serum in individuals who are particularly sensitive to horse protein.
Directions for use: 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 above drugs are not administered:
children and adolescents who have documented evidence of routine preventive vaccinations in accordance with age, regardless of the period that has passed since the next vaccination;
children and adolescents who have documentary evidence of a course of scheduled preventive vaccinations without the last age-related revaccination;
adults who have documented evidence of a full course of immunization no more than 5 years ago;
persons who, according to emergency immunological control, have a titer of tetanus toxoid in the blood serum higher than 1:160 according to RPGA;
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, conscripts and those who have served a specified period in the army, whose vaccination history is unknown, and there were no contraindications to vaccinations;
persons who, according to emergency immunological control, have a tetanus toxoid titer within the range of 1:20, 1:80 according to the RPGA (determination of antitetanus immunity (TDI), are carried out in cases where there is no documentary evidence of the patient’s immunization courses).
The full course of AS immunization for adults consists of two vaccinations with an interval of 30-40 days and revaccination after 6-12 months. With an abbreviated schedule, the full course of immunization includes a single vaccination with 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 PSCH (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 documented proof of vaccination;
persons who, according to emergency immunological control, have a tetanus toxoid titer of less than 1:20 according to RPGA.
It must be remembered that all persons who have received active-passive tetanus prophylaxis must be revaccinated with 0.5 ml AC or 0.5 ADS-M to complete the course of immunization in the period from 6 months to 2 years.
Prevention of anaerobic infection. To prevent clostridial anaerobic infection, anti-gangrenous serum is used.
Composition and release form: 1 ampoule of a polyvalent drug with a prophylactic dose contains 10,000 antitoxins against three types of gas gangrene pathogens (cl. perfringens, cl. novii, cl. septicum). The kit includes 1 ampoule of anti-gangrenosis serum and 1 ampoule of serum diluted 1:100 to determine sensitivity to horse protein.
Indications: gas gangrene (treatment and prevention), gangrenous diseases: postpartum anaerobic sepsis, lung gangrene, etc.
Directions for use and dosage:
for prophylactic purposes - if the intradermal test is negative, undiluted anti-gangrenosis 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 administered intramuscularly slowly.
for therapeutic purposes - administer 150,000 IU intravenously, drip-wise, diluting it 5 times with an isotonic sodium chloride solution. Before administering the serum, an intradermal test is performed to identify sensitivity to horse protein: 0.1 ml of diluted 1:100 serum (located in a separate 1 ml ampoule) is injected intradermally 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 no more than 0.9 cm with slight limited redness 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 effect), hemolysin (necrotizing and specific cardiotoxic effect, predetermining death), collagenase (lethal factor due to the lysis of protein structures), hyaluronidase (factor of penetration, spread of infection), fibrinolysin ( lyses fibrin, predetermines DIC syndrome), neuraminidase (destroys immune receptors on erythrocytes), 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 than others, predominantly cause the formation of large amounts 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, extensive necrotic changes, gas formation and high mortality from 27 to 90%.
However, the proportion of clostridia among all pathogenic anaerobes does not exceed 4-5%. There is a much larger and more 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 release of anaerobes ranges from 40 to 95%, depending on the nature and location 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, Campilobacter:
gram-positive cocci: Peptococcus, Peptostreptococcus, Ruminococcus;
gram-negative cocci: Vielonella.
In the development of purulent-inflammatory diseases of soft tissues, gram-negative bacteria (bacteroides, fusobacteria) and gram-positive cocci (peptococci and peptostreptococci) are of greatest importance. 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, β-hemolytic streptococcus, staphylococci, enterobacteria, etc.). The synergy between 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 exposure to oxygen. 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 ACI and ANI is very arbitrary, 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 primarily in the subcutaneous fatty 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. Soft tissue damage is often complicated by thrombophlebitis of the superficial and deep veins. Therefore, when examining patients, you should also pay attention to pain, tenderness and swelling outside the primary lesion.
The incubation period for anaerobic infection ranges from several hours to 7 days. The clinical picture is determined by general and local manifestations. An anaerobic infection is characterized by unusually severe burning pain at the primary site (injection site, wound, etc.), severe intoxication, an increase in body temperature to 39°C or more, tachycardia, a change in the patient’s psyche - euphoria, excitement, replaced by pessimism, depression, lethargy. In laboratory tests, the number of leukocytes increases from 12-2010 9 /l to 26.110 9 /l; shift of the leukocyte formula to the left; increase in leukocyte intoxication index (LII) from 3-7 to 21.4 arb. units; intoxication index (GPI) from 3-7 to 50.6 arb. units (at a norm of 1.3-1.6 conventional units); indicator of average mass molecules (MSM) more than 0.6-1.0 arb. units at a norm of 0.24 arb. units; decrease in the distribution index (DI) of MSM from 1.2 to 0.73 (with the norm being 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 1.5-2.510 12 /l.
Rapidly progressing intoxication quickly leads to the development of systemic failure, primarily cardiovascular, respiratory, hepatic, renal, endocrine, immune, and in especially severe cases – multiple organ failure. Energy metabolism, acid-base, water-electrolyte and protein balance were inevitably disrupted, hormonal deficiency developed, and serious imbalances arose in the coagulation and anticoagulation systems with the development of disseminated intravascular coagulation syndrome. When treating patients with anaerobic lesions, surgeons are often faced with comatose and collaptoid states against the backdrop of intensive complex therapy, the genesis of which can be extremely difficult to establish without sufficient laboratory support (hypo- and hyperglycemia, hypokalemia, blood sugar imbalance, 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 phase of severe toxemia, this control should be carried out in a monitoring mode.
At the earliest stages of the disease, there is a discrepancy between the severity of toxemia and the paucity 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 only be counted on if complex treatment is started immediately. The diagnosis of this pathology in a wide medical network should be based on clinical specific manifestations of anaerobic infection, determined by the ecology of the pathogens, their metabolism and pathogenicity factors.
There is always pronounced swelling around the wound or injection, which does not leave a mark after pressing with a finger. Tissue swelling is confirmed by clearly defined depressions at the hair root and the symptom of “cutting in” of the ligature.
In the affected area, patients report very strong burning or bursting pain, which is not relieved by analgesics and tends to intensify over time. With banal aerobic flora, the pain is moderate.
The skin in the area of inflammation is tense, the color is often pale and shiny. Much less often, the skin against the background of edema is hyperemic without clear boundaries with a tendency to quickly spread in all directions. When the fascia is involved in the inflammatory process and thrombosis of small vessels (usually veins) develops, areas of darkening or necrosis may appear on the skin, and subepidermal dark cherry blisters may form.
Palpation of the presence of gas in the subcutaneous tissue (subcutaneous crepitus), in the intermuscular spaces or muscle sheath formations (gas movement during deep palpation) often confirms the diagnosis. Gas accumulates in tissues because anaerobic metabolism releases hydrogen, nitrogen and methane, which are poorly soluble in water. Gas formation can be detected somewhat earlier and more reliably by x-ray (air bubbles in soft tissues) and by ultrasound. A clinical, radiological and ultrasound examination over time seems justified. At even earlier stages, small gas bubbles that are not clinically apparent can be seen in the exudate during drainage of abscesses or at the time of opening and excision of tissue. Naturally, the phenomenon of gas formation in tissues can be clearly taken into account in the absence of signs of direct entry into tissues during injury, 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 typical for anaerobic clostridial infection with a predominance of Cl in the microbial landscape. perfringens. In practice, forms of anaerobic non-clostridial infection currently predominate, in which gas formation is scanty 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. While waiting for his appearance, you can lose the patient. In these cases, it is necessary to pay attention to other clinical signs of anaerobic inflammation. Among our patients, the classic accumulation of gas in soft tissues with “snow crunch” palpation, the presence of clear foci of darkening in the tissue, in the intermuscular sections, along the wound canal on radiographs, 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 fairly constant symptom indicating the presence of anaerobes in tissues is the unpleasant putrid odor of exudate. The previously attributed property of producing a similar odor to E. coli turned out to be erroneous. Cultivation of isolated anaerobes in anaerostats with absolute consistency confirmed their involvement in the formation of unpleasant-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 areas of infection, dead tissue is often found in the form of structureless debris that is gray-dirty or gray-green in color, sometimes with black or brown areas. They do not have clear boundaries and specific forms. Putrefactive tissue damage is explained by the peculiarities of the metabolism of anaerobes - one of the elements of decay is the process of anaerobic oxidation of the protein substrate.
The color and character of the exudate have very specific features. It can be scanty, gray-green or brown in color. Coloring may not be uniform. The exudate is usually very liquid; in the tissue layers it can be abundant, but for muscle infections, scant diffuse penetration of tissue is more typical. Over time, with the addition of aerobic flora, the discharge from the wound can become mixed, and then purulent - a thicker consistency, dark yellow in color, homogeneous, odorless. It should be emphasized that the distinctive signs of exudate are most clearly identified in the early stages of the disease. The discovery at the time of opening or revision of a 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, i.e. caused by the patient's own microflora. This leads to their clinical feature - proximity to the natural habitats of anaerobes - the digestive tract, respiratory tract, hollow organs. Practice shows that anaerobic and mixed lesions more often occur with injuries to the gastrointestinal tract with damage to the mucous membrane, with wounds and scratching in the perineum, with injections in the buttock areas, with animal and human bites, as well as on the hand after blows to the teeth.
Anaerobic infections should be suspected in cases where it is not possible to isolate any pathogen using the usual culture method or when the number of isolated bacteria does not correspond to what is visible in smears under a microscope, as well as if the patient has 2-4 or more of the described local symptoms.
Anaerobic infection is one of the types of wound infection and is one of the most severe complications of injuries: compartment syndrome, frostbite, wounds, burns, etc. The causative agents of anaerobic infection are gram-negative bacteria (anaerobic gram-negative bacilli, AGOB), living in conditions of severely limited or completely absent oxygen access. The toxins released by anaerobic bacteria are very aggressive, highly penetrating and affect vital organs.
Regardless of the localization of the pathological process, anaerobic infection is initially considered as generalized. In addition to surgeons and traumatologists, doctors of various specialties encounter anaerobic infection in clinical practice: gynecologists, pediatricians, dentists, pulmonologists and many others. According to statistics, anaerobes are found in 30% of cases of the formation of purulent foci, but the exact proportion of complications caused by the development of anaerobes has not been determined.
Causes of anaerobic infection
Anaerobic bacteria are classified as opportunistic and are part of the normal microflora of the mucous membranes, digestive and genitourinary systems and skin. Under conditions that provoke their uncontrolled reproduction, an endogenous anaerobic infection develops. Anaerobic bacteria that live in decomposing organic matter and soil, when introduced into open wounds, cause exogenous anaerobic infection.
With respect to oxygen, anaerobic bacteria are divided into facultative, microaerophilic and obligate. Facultative anaerobes can develop both under normal conditions and in the absence of oxygen. This group includes staphylococci, E. coli, streptococci, Shigella and a number of others. Microaerophilic bacteria are an intermediate link between aerobic and anaerobic; oxygen is necessary for their life, but in small quantities.
Among obligate anaerobes, clostridial and non-clostridial microorganisms are distinguished. Clostridial infections are exogenous (external). These are botulism, gas gangrene, tetanus, food poisoning. Representatives of non-clostridial anaerobes are causative agents of endogenous purulent-inflammatory processes, such as peritonitis, abscesses, sepsis, phlegmon, etc.
The development of anaerobic infection is facilitated by tissue damage that allows the pathogen to enter the body, a state of immunodeficiency, massive bleeding, necrotic processes, ischemia, and some chronic diseases. Invasive manipulations (tooth extraction, biopsy, etc.) and surgical interventions pose a potential danger. Anaerobic infections can develop due to contamination of wounds with soil or the entry of other foreign bodies into the wound, against the background of traumatic and hypovolemic shock, irrational antibiotic therapy, which suppresses the development of normal microflora.
Characteristics (species), pathogens
Strictly speaking, anaerobic infections include pathological processes caused by the vital activity of obligate anaerobes and microaerophilic organisms. The mechanisms of development of lesions caused by facultative anaerobes are somewhat different from typically anaerobic ones, but both types of infectious processes are clinically very similar.
Among the most common pathogens of anaerobic infection are;
- clostridia;
- propionibacteria;
- bifidobacteria;
- peptococci;
- peptostreptococci;
- sarcins;
- bacteroides;
- fusobacteria.
In the vast majority of anaerobic infectious processes occur with the joint participation of anaerobic and aerobic bacteria, primarily enterobacteria, streptococci and staphylococci.
The most complete classification of anaerobic infections, optimally suitable for use in clinical practice, was developed by A. P. Kolesov.
According to microbial etiology, clostridial and non-clostridial infectious processes are distinguished. Non-clostridial ones, in turn, are divided into peptococcal, fusobacterial, bifidobacterial, etc.
Based on the source of infection, anaerobic infections are divided into endogenous and exogenous.
According to the species composition, infectious agents are divided into monobacterial, polybacterial and mixed. Monobacterial infections are quite rare; in the vast majority of cases, a polybacterial or mixed pathological process develops. Mixed infections are defined as infections caused by an association of anaerobic and aerobic bacteria.
Based on the location of the lesions, infections of bones, soft tissues, serous cavities, bloodstream, and internal organs are distinguished.
Based on the prevalence of the process, the following are distinguished:
- local (limited, local);
- regional (unlimited, prone to distribution);
- generalized or systemic.
Depending on the origin, the infection may be community-acquired or hospital-acquired.
Due to the occurrence of anaerobic infections, spontaneous, traumatic and iatrogenic infections are distinguished.
Symptoms and signs
Anaerobic infections of various origins have a number of common clinical signs. They are characterized by an acute onset accompanied by an increase in local and general symptoms. Anaerobic infections can develop within several hours, the average incubation period is 3 days.
In anaerobic infections, the symptom of general intoxication is characterized by a predominance of symptoms over the manifestations of the inflammatory process at the site of infection. Deterioration of the patient's condition due to developing endotoxemia often occurs before visible signs of the local inflammatory process appear. Symptoms of endotoxicosis include:
- headache;
- general weakness;
- inhibition of reactions;
- nausea;
- tachycardia;
- fever;
- chills;
- rapid breathing;
- cyanosis of the extremities;
- hemolytic anemia.
Early local symptoms of wound anaerobic infection:
- bursting severe pain;
- soft tissue crepitus;
- emphysema.
The pain that accompanies the development of anaerobic infection is not relieved by analgesics, including narcotics. The patient's body temperature rises sharply, the pulse quickens to 100-120 beats per minute.
Liquid purulent or hemorrhagic exudate emerges from the wound, heterogeneously colored, with gas bubbles and fatty inclusions. The smell is putrid, indicating the formation of methane, nitrogen and hydrogen. The wound contains gray-brown or gray-green tissue. As intoxication develops, disorders of the central nervous system occur, including coma, and blood pressure decreases. Against the background of anaerobic infection, the development of severe sepsis, multiple organ failure, and infectious-toxic shock, leading to death, is possible.
Non-clostridial pathological processes are indicated by the release of brown pus and diffuse tissue necrosis.
Clostridial and non-clostridial anaerobic infections can occur in fulminant, acute or subacute form. Fulminant development is said to occur if the infection develops within the first 24 hours after surgery or injury; An infectious process that develops within 4 days is called acute; the development of the subacute process is delayed by more than 4 days.
Diagnostics
The peculiarities of the development of anaerobic infections often leave doctors no choice but to diagnose the pathology based on clinical data. The diagnosis is supported by a foul odor, tissue necrosis, as well as the localization of the infectious focus. It should be noted that with subacute development of the infection, the smell does not appear immediately. Gas accumulates in the affected tissues. The ineffectiveness of a number of antibiotics indirectly confirms the diagnosis.
The sample for bacteriological examination must be taken directly from the source of infection. It is important to exclude contact of the taken material with air.
Biological materials obtained by puncture (blood, urine, cerebrospinal fluid) and tissue fragments obtained by puncture conicotomy are suitable for identifying anaerobes. The material intended for research must be delivered to the laboratory as quickly as possible, since obligate anaerobes die when exposed to oxygen and are replaced by microaerophilic or facultative anaerobes.
Treatment of anaerobic infection
The treatment of anaerobic infection requires a comprehensive approach, including surgery and conservative treatment methods. Surgical intervention when an anaerobic pathological process is detected should be performed without delay, since the chances of saving the patient’s life are rapidly decreasing. Surgical treatment is reduced to opening the infectious focus, excision of necrotic tissue, open drainage of the wound with rinsing with antiseptic solutions. Depending on the further course of the disease, the need for repeated surgery cannot be ruled out.
In the most severe cases, it is necessary to resort to disarticulation or amputation of the affected limbs. This is the most radical method of combating anaerobic infection and is used in extreme cases.
Conservative general therapy is aimed at increasing the body's resistance, suppressing the vital activity of the infectious agent, and detoxifying the body. The patient is prescribed broad-spectrum antibiotics and intensive infusion therapy. If necessary, anti-gangrenous antitoxic serum is used. Extracorporeal hemocorrection, hyperbaric oxygenation, and ultraviolet therapy are performed.
Forecast
The prognosis is cautious, since the outcome of anaerobic infection depends on the timeliness of detection and initiation of treatment, as well as the clinical form of the pathology. In some forms of anaerobic infection, death occurs in more than 20% of cases.
Prevention
Preventive measures include the removal of foreign bodies from the wound, strict implementation of antiseptic and aseptic measures during operations, and timely postsurgical treatment of the wound appropriate to the patient’s condition. If there is a high risk of anaerobic infection, the patient is prescribed antimicrobial and immune-strengthening treatment in the postoperative period.
Which doctor should I contact?
The main treatment for anaerobic pathologies is surgical. If you suspect an anaerobic infection, you should immediately contact a surgeon.
