Radiant mushrooms. Actinomycosis: treatment in humans

Actinomycosis is a chronic, slowly progressive infectious disease of humans and animals; caused by radiant fungi - actinomycetes; characterized by granulomatous lesions of tissues and organs, the development of dense, often taut infiltrates, the formation of abscesses, fistulas and scars.

The main route of infection is considered endogenous - due to the activation of actinomycetes - the usual inhabitants of the skin and mucous membranes. The pathogen can be introduced through the mucous membrane of the oral cavity (including the tonsils), the gastrointestinal tract (in particular, the intestines, for example, the ileocecal region), lungs, skin; less often - in other ways (urethra, eyes, cervix). Its penetration deep into the surrounding tissues causes the development of a primary lesion such as an infectious granuloma. Hematogenous dissemination of actinomycetes from mycosis foci already present in the body is possible. In healthy people, as noted, actinomycetes can occur in a saprophytic state - in the mouth, carious teeth, dental granulomas, tonsil crypts (including with local inflammatory processes - odontogenic, rhinotonsillar and other various diseases), as well as the respiratory tract, intestines.

It should be noted that in nature there are many actinomycetes (more than 300 species), including the soil, but not all of them and only under certain conditions can be pathogenic. It is figuratively noted that "actinomycetes are not yet actinomycosis." In a healthy body, the fungus is in unfavorable conditions and usually lyses.

Damage to the oral mucosa.

Its transformation from a saprophytic state to a pathogenic one is facilitated by:

• helminthic invasion.
• exposure to concomitant microflora, especially in an immunosuppressive organism.
• diseases of the nervous system, blood vessels.
• sensitization, repeated ingestion of the fungus and even alimentary errors (fatty foods).
• of particular importance in the occurrence of the disease is given to trauma (damage to the mucous membrane in the mouth, worms in the intestines).

And at present, an exogenous route of infection is not excluded. The widespread distribution of actinomycetes in the air, soil, and plants can be one of the factors of exogenous infection (for example, when it enters an open wound surface, if it is injected with plants on which fungi are located). It was believed that infection of humans (and animals) can occur by the introduction of actinomycetes into the damaged mucous membrane, for example, when chewing actinomycete-infected cereals. There is very demonstrative evidence of the alleged transmission of actinomycosis from a sick person or animal to healthy persons (but these cases represent rare exceptions). With a significant distribution of actinomycetes in nature, actinomycosis is relatively rare, not distinguished by noticeable contagiousness.

Symptoms of actinomycosis:

It is assumed that the incubation period for actinomycosis varies widely and ranges from 9-20 days to 11-22 years (more often in the range from 1-2 years to 10 years). The clinical manifestations of actinomycosis are highly variable. In this case, all organs and tissues can be affected by the mycotic process - skin, mucous membranes, bones, joints, internal organs, and the nervous system. There are stages of actinomycosis: initial, "woody infiltrate", abscesses and fistulas, metastases.

Actinomycosis of the maxillofacial region:

The most common and characteristic actinomycosis occurs in the maxillofacial region (including the maxillary sinuses) and neck (cervical actinomycosis occurs in up to 80% of cases). With actinomycosis of the head and neck, painful dense infiltrates (fixed or inactive, soldered to the surrounding tissues) appear at the sites of penetration of the radiant fungus; nodes - dense, bluish-red color - with subsequent softening, opening and the formation of long-term non-healing fistulas (with purulent bloody discharge). In place of festering infiltrates, ulcers and scars form. The abscessing form of actinomycosis is also known (it proceeds as phlegmon, abscesses).

In many patients, actinomycosis does not cause significant subjective sensations (including pain); however, sharp, burning, "fiery" pain in the fistula area occurs on palpation. There may be lesions in the oral cavity (including on the tongue), salivary glands, masticatory muscles (trismus develops, facial asymmetry), bones; in the future, the process sometimes extends to the adnexal cavities, the region of the skull, the surrounding areas of the skin and subcutaneous tissue. Lymph nodes are usually not involved; however, with their defeat, the course of actinomycosis is protracted.

With thoracic actinomycosis(about 13-15% of cases) the process captures the organs of the chest cavity and chest wall - with the release of fistulas on the skin of the chest, the destruction of intercostal muscles, ribs, vertebrae (periostitis or osteomyelitis of a destructive type with sequesters). With actinomycosis of the lungs, weakness, loss of appetite, weight loss increase; patients are worried about a painful cough with scanty sputum, hemoptysis. Less commonly, the disease begins acutely, according to the type of banal pneumonia, taking a chronic course in the future. Sometimes lung abscesses form. Characteristic is the involvement in the process of the pleura - in the form of exudative pleurisy or empyema. Known forms of actinomycosis in the form of bronchiectasis.

With abdominal actinomycosis(about 3% of cases) the organs of the abdominal cavity and tissues of the abdominal wall are affected. The process usually spreads through the retroperitoneal tissue. The first manifestations are often noted in the gastrointestinal tract (more often in the ileocecal region). Other parts of the intestine, the stomach, are less commonly affected. The formation of fistulas is characteristic. Differential diagnosis should be carried out with neoplasms, abscesses of various etiologies, echinococcosis, etc.

There are also actinomycosis of the pelvic organs and genitourinary areas, pararectal (paraproctitis), sacrococcygeal (with bone damage), gluteal. Cases of infection generalization are described - with the development of actinomycotic brain abscesses, meningoencephalitis; in rare cases - corneal lesions, etc.

More on fungal infections:

The clinical diagnosis of actinomycosis should be confirmed:

1) bacterioscopic studies; at the same time, the detection of drusen of the radiant fungus is decisive for the diagnosis. The material for the study is: punctates, sputum, biopsy specimens, and especially the discharge of dense infiltrates, fistulous passages and pus. For research, white or yellowish dense grains (“grains”) are removed from the material and in a crushed form - 15-20% solution of caustic sodium or potassium is added for maceration, the glass is slightly heated, a cover glass is applied.

Microscopy of unstained preparations is carried out under high magnification of the dry system. At the same time, characteristic drusen are visible - densely intertwined thin threads of mycelium in the center of the conglomerate; along the periphery - flask-shaped formations are radially arranged, sharply refracting light (they are the final “bloatings” of the mycelium). When stained according to Gram, the mycelium of the fungus is purple (stained with gentian violet), and the flask-shaped "bloatings" are red (discolored and perceive magenta stain). However, even with a typical clinical picture, drusen are not always detected, but thin branching filaments of mycelium (possessing acid resistance) are detected - the so-called. atypical actinomycosis of Berestnev (differs from the typical absence of drusen in the pus - without any clinical differences). 2) Microscopic studies are supplemented by cultural ones (they sow "grains" containing elements of the fungus).

3) Studies are also recommended: purulent discharge using a direct test of fluorescent antibodies; ultrasound scanning; CT scan; radioisotope examination (may help in the detection of "silent" abdominal abscesses).

4) In the diagnosis of actinomycosis, great importance is attached to histopathological studies; at the same time, it is possible to detect drusen of the radiant fungus in the affected tissue. Differentiate actinomycosis - with tuberculous ulcers (scrofuloderma, lupus), syphilitic gums, chronic deep pyoderma, tumors, deep mycoses, osteomyelitis of a different etiology and other suppurative processes. In this case, one should take into account the most characteristic clinical signs of actinomycosis (a very high density of nodes and infiltrates, their tendency to open and form fistulas), and most importantly, the detection of drusen of the radiant fungus (identification of drusen was considered an obligatory criterion for diagnosing actinomycosis).

Treatment of actinomycosis.

Treatment of actinomycosis includes: specific immunotherapy, antibiotics, sulfonamides, tonic and stimulants, vitamins, surgical and physical methods. Complex treatment of actinomycosis can be carried out sequentially:

Stage 1 — combined use of actinolysate and antibiotics. The main specific immunodrug for actinomycosis is actinolysate; entered in 2 ways:

1. i / m 3 ml 2 r / week, for a course of 20-25 injections; after 1-1.5 months, the treatment is repeated;
2. in / to, starting from 0.5 ml to 2 ml 2 r / week, courses of 3 months with an interval of 1-1.5 months.

After clinical recovery, 2-3 courses of anti-relapse therapy are carried out. It is noted that the intradermal method of administration of actinolysate is more efficient and economical than the intramuscular one. Actinolysate is one of the most effective means of treating actinomycosis (various clinical forms and localizations). The use of antibiotics is one of the leading places in the treatment of actinomycosis; prescribe tetracyclines (unidox-solutab, doxibene, vibromycin, oxytetracycline, etc.); penicillins (long-term and in high doses: penicillin G 10-20 million units / day intravenously, for 4-6 weeks; then they switch to phenoxymethylpenicillin inside 2-4 g / day, 6-12 months); you can use ampicillin intravenously at 50 mg / kg / day (4-6 weeks) - followed by its replacement with oral forms - amoxicillin at 0.5 g / day inside, 6 months. It is possible to use other antibiotics (erythromycin, streptomycin, clindamycin, ristocetin, etc.). 3rd generation cephalosporins (ceftriaxone) are recommended. Sometimes treatment is combined with isoniazid, the course dose is 70-120 g.

Stage 2 includes the appointment of sulfonamides (course, dose 60-100 mg), incl. combined agents are used (bactrim, groseptol, berlotsid, etc.). Sulfadimezin is prescribed at 4-6 g / day (course 1-5 weeks). During this period, physical methods of treatment (phonophoresis, electrophoresis of potassium iodide, UHF), autohemotherapy are used.

3rd stage - the use of iodine preparations - potassium iodide orally in the form of a 25% solution (in milk or meat broth); inhalation - with actinomycosis of the lungs. At all stages, general strengthening and stimulating therapy is carried out (vitamins C, group B, biostimulants; according to indications - immunocorrectors, gamma globulin, interferon inducers). Food should be rich in proteins, vitamins. In severe cases, detoxification therapy is performed; apply blood transfusions of 200 ml 1 r / week. According to indications, surgical intervention is performed (opening and drainage of abscesses, excision of fibrous-changed tissues).

The course of the disease is usually 1-3 years; without treatment, the process progresses, causing destructive changes. After clinical recovery, patients with actinomycosis should be observed for at least 2 years (due to the possible recurrence of the disease). Prevention of actinomycosis consists in the rehabilitation of the oral cavity, the fight against injuries and the timely treatment of microtraumas (ioddicerin, 5% alcohol iodine solution) - especially among rural residents.

ACTINOMYCOSIS, ACTINOBACILLOSIS AND RELATED DISEASES

Part /1 / 2 / 3 /

1. General view
2. Actinomycosis
3. Other diseases caused by fermenting actinomycetes
4. Diseases caused by aerobic actinomycetes
5. Nocardiac infections
6. Actinomycetoma
7. Other diseases caused by aerobic actinomycetes
8. Diseases caused Rhodococcus spp.
9. Diseases caused Gordonia spp.
10. Diseases caused Tsukamurella spp.
11. Diseases caused Amycolatopsis and Pseudonocardia spp.
12. Diseases caused Oerskovia spp.
13. Dermatophilosis
14. Diseases caused Actinobacillus spp.
15. Actinomycetes as allergens

SECTION APPENDIX:

1. Short-term treatment of actinomycosis: two case reports and a review of the literature (Selvin S. Sudhakar and John J. Ross)
2. literature review "Actinomycosis of the genital organs in women" (ed. Mirzabalaeva A.K.) journal "Problems of Medical Mycology" -2000-V.2 (2) .- P.11-16;
3. Abdominal actinomycosis (literature review and description of two cases).
4. Optimal duration of intravenous and oral administration of antibiotics in the treatment of thoracic actinomycosis.
5. Actinomycosis of the pelvic organs. Is long-term antibiotic treatment necessary?

General view

Actinomycosis, actinobacillosis, actinomycetoma and nocardiosis are diseases that are not related in terms of etiology, epidemiology and therapy, but there are good reasons to consider them together, since they have a common history and nomenclature origin, as well as similar clinical and pathological manifestations. The taxonomic relationships between some of their causal agents are also similar.

The history of actinomycosis dates back to the early days of bacteriology. In 1877, the German veterinarian Otto Bollinger discovered that chronic tumor-like lesions of the jaws of cattle, thought of as a kind of sarcoma, contain small, opaque, yellowish, granular particles. Because their structure resembled a group of crystals, he called them "druze". Drusen were formed from filament-like, branching, mushroom-like structures, subsequently characterized as Gram-positive. The botanist Carl O Harz (1877) believed that this was a new type of mold and proposed a generic and specific designation. Actinomyces bovis(radiant mushrooms, from the Greek aktis = ray; mykes = mushroom) due to the striking ray divergence of the filaments in the granules. He also first introduced the term "actinomycosis" for this disease.

The first detailed description of such pathological conditions in humans was published by the Berlin surgeon James Israel in 1878. About a decade later, it was established that the most characteristic human pathogen, now called Actinomyces israelii or Actinomyces gerencseriae, and an animal pathogen A. bovis are anaerobes, or at least facultative anaerobic capnophiles, bacteria that grow best in high CO2 (Bujwid 1889, Mosselman and Lienaux 1890). Only a few decades later it was established that the causative agents of human and "bovine" actinomycosis are separate species and that they are true, albeit filamentous, bacteria and not fungi, and that they were the first representatives of a large and heterogeneous group of Bacteria, now belonging to orders Actinomycetales and Bifidobacteriales subclass Actinobacteridae in a newly defined class Actinobacteria(Stackebrandt, Rainey and Ward - Rainey 1997), but still often referred to simply as "actinomycetes".

Lignieres and Spitz in 1902 described a new bovine disease in Argentina that clinically and pathologically resembled bovine actinomycosis. Organisms cultured from the respective lesions were tiny, short gram-negative bacterial rods that differed markedly from A. bovis. Due to the similarity between the clinical presentations of the two diseases, the pathogen was first named "Actinobacillus" and then officially designated as Actinobacillus lignieresii(Brumpt 1910).

Before the anaerobic nature of the pathogens of human and animal actinomycosis was established, many attempts were made to grow microorganisms under aerobic conditions. In an extensive study of cases of actinomycosis in humans and cattle, Bostroem (1891) isolated filamentous microorganisms on aerobic gelatin or agar, which he regarded as pathogenic and to which he gave the name " Actinomyces bovis He also observed grain awns at the center of actinomycotic lesions and isolated culturally similar aerobic filamentous microorganisms from grass, grain, and other plant materials. In this regard, Bostroem concluded that grass or grain are exogenous sources of actinomycotic infection and that chewing grass or grain could cause actinomycotic damage.This version persisted for a long time even after the studies of Naeslund (1925, 1931) proved that A. israelii is part of the innate microflora of the human oral cavity, which is not found in the environment, and thus the source of actinomycosis is always endogenous.

By the end of the 19th century, several investigators had identified pathogenic aerobic actinomycetes similar to those of actinomycosis isolated by Bostroem. Nocard (1888) described an aerobic filamentous microorganism in "farcin du boeuf", a cattle disease in Guadeloupe. This stimulus is called Nocardia farcinica Trevisan (1889). A similar branching bacterium was isolated from an affected human lung by Eppinger (1891), and this pathogen was subsequently designated as Nocardia asteroides Blanchard (1896). Another filamentous branching bacterium, first identified as " Streptothrix madurae", was isolated by Vincent (Vincent, 1894) from tumor-like lesions in India, called the "Madure foot". This organism was later named " Nocardia madurae"and is now known as Actinomadura madurae(Lechevalier and Lechevalier 1970).

Since Bollinger's report, numerous additional genera and varieties of aerobic and anaerobic actinomycetes have been described. For the most part, these were harmless inhabitants of the environment or body surfaces of humans and animals, and only a few could act as a pathogen in both humans and animals. This applies not only to some members of traditional families Actinomyces and Nocardia, but also to varieties of genera Bifidobacterium, Propionibacterium, Oerskovia, Gordonia, Rhodococcus, Tsukamurella, Actinomadura, Nocardiopsis, Streptomyces, Dermatophilus, Thermoactinomyces, Saccharopolyspora (Faenia), Saccharomonospora and Thermomonospora. Despite the growing spectrum of pathogenic actinomycetes, it would hardly be appropriate to add, in addition to actinomycosis, nocardiosis, dermatophilosis, numerous further etiological designations such as propionibacteriosis, rhodococcosis, tsukamurellosis, etc. On the other hand, for the sake of clarity, it would also not be entirely correct to use the term "actinomycosis" for any type of infection caused by actinomycetes, as was common practice in the past. Similarly, the term "nocardiosis" does not cover all types of nocardial infections, nor infections caused by other anaerobic actinomycetes. Thus, the classic disease designations "actinomycosis" and "nocardiosis" should be retained to refer to a specific, clinically and etiologically defined disease with a characteristic clinical presentation.

Diseases caused by fermenting actinomycetes

Carbohydrate fermenting anaerobic or capnophilic actinomycetes belonging to the families Actinomycetaceae, Propionibacteriaceae or Bifidobacteriaceae, act as etiological agents in various diseases in humans and animals. Among them, actinomycosis is the most characteristic manifestation of the disease. Other diseases that can be caused by fermenting actinomycetes: dental caries and periodontitis, lacrimal canaliculitis and other eye infections; infections associated with the use of intrauterine contraceptives and vaginal uterine rings, other inflammatory processes in humans, such as mastitis, peritonitis, pleurisy, septic abortion, abscesses, and also a wide variety of purulent lesions in animals.

Actinomycosis

Actinomycosis is a subacute or rather chronic granulomatous disease that usually causes suppuration and abscess formation and tends to form fistulous tracts. The disease occurs in humans and animals. In addition to classical pathogens A. bovis and A. israelii, actinomycotic lesions can cause a diverse number of species of other enzymatic actinomycetes. Most of these agents belong to the genus Actinomyces, but some are members of the genus Propionibacterium or Bifidobacterium. In addition, all typical actinomycotic lesions contain a variety of bacteria in addition to pathogenic actinomycetes. Thus, the term "actinomycosis" defines a polyetiological inflammatory syndrome rather than simply a disease related to a single pathogenic microorganism. In order to avoid introducing additional etiological terms and to remain bacteriologically correct, it has been proposed to designate a group of closely related inflammatory processes with the term "actinomycosis" in the plural (Schaal and Beaman 1984, Schaal 1996).

Actinomycosis in humans

Despite significant similarities in pathology, pathogenesis, and epidemiology, human and animal actinomycosis differ from each other in several important respects. Various species of actinomycetes are responsible for infections in humans and animals, and furthermore, bone involvement is rarely seen in humans but very common in animals (Slack and Gerencser 1975).

Clinical manifestations of actinomycosis

The initial actinomycotic lesions usually develop in the tissues adjacent to the mucous membranes, which are the natural habitats of the causative agents. The following areas are most often affected: cervicofacial, thoracic and abdominal. Rarely, the skin, bones, or central nervous system (CNS) may also be involved (Slack and Gerencser 1975, Pulverer and Schaal 1984, Schaal and Beaman 1984, Schaal and Pulverer 1984, Schaal 1996). After penetration of the pathogen into the tissues, the infection tends to progress slowly, regardless of the natural boundaries of the organ. Occasionally, hematogenous spread is seen, in which the CNS (brain abscess) or natural cavities (empyema) may be involved. There is a characteristic tendency for both remission and exacerbation of symptoms, regardless of antibiotic therapy. Due to the fact that actinomycosis in humans are endogenous infections, it is difficult or impossible to determine their incubation period. It is believed that approximately 4 weeks pass before the first clinical signs appear, but numerous reports suggest that this period may be much longer or much shorter.

cervicofacial actinomycosis

In the vast majority of cases, actinomycotic infection affects the face, neck, or both - the so-called cervicofacial region (data collected in Germany; see Table 1), but the numbers may vary in different geographical areas, especially in USA.

Table 1 Localization of actinomycosis in humans

Data collected at the Institute of Hygiene, University of Cologne, 1969-84, and at the Institute for Medical Microbiology and Immunology, University of Bonn, Germany, 1984-95.

Actinomycotic lesions are often preceded by a history of caries and tooth decay, tooth extraction, jaw fracture, periodontal abscess, mucosal injury by foreign bodies (bone splinters, fish bones, grass or grain awns), or tonsil suppuration. It should be remembered that traumatic factors, local or general predisposing conditions - do not necessarily occur in all cases or may be missed when taking an anamnesis.

In cervicofacial actinomycosis, according to the analysis of 317 patients, the following tissues were most often involved in the process: adjacent to the lower jaw (53.6%), cheek (16.4%), chin (13.3%), mandibular branch and angle (10.7%) , maxilla (5.7%) and jaw joint (0.3%) (Herzog 1981). Other sites that are less commonly affected are the neck, mastoid, sinuses, parotid, thyroid, tongue, lips, nasal septum, and ears (Slack and Gerencser 1975, Kingdom and Tami 1994). Direct involvement of bone and regional lymph nodes is very rare, but periostitis and post-traumatic osteomyelitis with fermenting actinomycetes are not uncommon (11.7% of cases reported by Herzog 1981).

Primary cervicofacial actinomycotic lesions present either as acute, predominantly odontogenic, abscesses, or very acute forms of panniculitis, or as slow-onset, hard, reddish, or pallid inflammatory infiltrates (Lentze 1969, Pulverer and Schaal 1978, Schaal 1979, 1981, 1996). Whereas, although chronic infiltrates are usually painless and acute forms of infection are painful, they can all lead to trismus of mastication when the process forms near the temporomandibular joint.

To lead to rapid and complete healing, only a surgical incision and drainage in the vast majority of cases is not enough. Acute and especially chronic cases tend not to heal without specific antibiotic therapy. At best, there is a temporary regression of signs, after which relapses may develop after a few weeks or months. The longer both forms of actinomycosis persist, the sooner similar and very characteristic late signs of this disease develop in both cases. They include: regression and scarring of the central purulent focus, progression of firm, painless, pallid infiltrates on the periphery, the formation of multiple areas of softening and fistula formation. The latter appear spontaneously or form at the site of the surgical incision and, together with multiple abscesses, form a multi-chamber system of cavities in the affected tissue, which responds poorly to conventional therapy, including the administration of "standard" antibiotics, and shows a clear tendency to relapse after a temporary regression of inflammatory signs. . Untreated or inappropriately treated, cervicofacial actinomycosis progresses slowly, even across organ boundaries, and can become life-threatening if it invades the cranial cavity, mediastinum, or large blood vessels (Herzog et al., 1984). Discharge from fistulas and pus from abscesses is usually yellowish in color and thicker than serous discharge and often contains particles originally called "drusen", or often referred to as "sulfur granules".

Thoracic actinomycosis

Thoracic lesions in actinomycosis are much less common than the cervicofacial form. The formation of the process is usually preceded by aspiration of pathogenic material from the oral cavity, for example, plaque or calculus, the contents of the tonsil crypt or a foreign body contaminated with oral microflora, including pathogenic actinomycetes. Sometimes, this form of the disease develops due to local spread of the cervicofacial process, perforation of the diaphragm due to damage to the abdominal cavity, or hematogenous spread from any distant site of infection (Slack and Gerencser 1975).

First of all, thoracic actinomycosis may appear as a mediastinal tumor or bronchopneumonic infiltrate, necrotizing pneumonia, or lung abscess (Slack and Gerencser 1975, Schaal and Beaman 1984, Morris and Sewell 1994). Radiographs show individual dense or multiple shadows in which cavities may form. Early on, the main symptoms are chest pain, fever, cough with or without sputum, and weight loss, but hemoptysis is uncommon. Later, the infection may progress to pleural empyema, pericarditis, or chest wall involvement. If the diagnosis is late or treatment is inadequate, late signs may include extensive subcutaneous chest wall abscesses, paravertebral or pelvic abscesses that form in the groin and are emptied by pus containing large amounts of actinomycotic drusen.

Abdominal actinomycosis

Actinomycotic lesions of the abdominal cavity and anorectal region are quite rare (Table 1). Their development is associated with acute perforation of internal organs (appendicitis, diverticulitis, cryptitis, various peptic ulcers), surgical or other traumatic injuries, including lesions by swallowed bone fragments or fish bones.

Another source of pelvic and abdominal actinomycotic infections has recently been identified. It turned out that in 10-20% of women with intrauterine contraceptives or vaginal uterine rings, the uterus and cervical canal are colonized by a mixed bacterial flora, which includes potentially pathogenic fermenting actinomycetes (Gupta, Hollander and Frost 1976, Gupta, Erozan and Frost 1978, Eibach and others. 1989, 1992, Schaal and Lee 1992, Chatwani and Amin-Hanjani 1994) and other predominantly anaerobic bacteria (Schaal and Lee 1992). They practically do not occur in women who do not use these devices. This colonization may serve as an initial site for the development of aggressive pelvic actinomycosis and may even be the source of hematogenous metastatic hepatic or intracranial actinomycotic abscesses (Gupta, Erozan and Frost 1978).

The initial signs of abdominal actinomycosis are usually unexpressed and indefinite. They include: fever, malaise, weakness, and pain that slowly but progressively increase. In the course of the process, it usually resembles slowly progressive malignant-like tumors, such as cancer of the stomach, colon and rectum, anorectal region, or cervix (Stein and Schaal 1984, Schaal 1985b, Ewig et al. 1993, Alvarado-Cerna and Bracho-Riquelme 1994, Skoutelis et al. 1995). Large subcutaneous abscesses, extensive pallid indurations, or fistulas may be observed, the discharge of drusen from which is often the first characteristic sign of the disease (Schaal and Beaman 1984). Without effective treatment, abdominal actinomycosis may spread to any adjacent tissue or organ, including the liver, spleen, kidney, fallopian tubes, ovaries, uterus, testicles, bladder, rectum, or abdominal wall (Slack and Gerencser 1975, Khalaff, Srigley, and Klotz 1995, Mmller-Holzner et al. 1995).

Actinomycosis of the central nervous system

Actinomycosis of the brain and spinal cord is very rare, perhaps due to the now more effective antibiotic therapy that prevents hematogenous or direct spread of infection (Table 1). It is these mechanisms that are predominantly responsible for CNS involvement, especially when the primary lesion is located in the lungs or in the abdomen (Slack and Gerencser 1975, Jamjoom, Jamjoom and al-Hedaithy 1994, Voisin et al. 1998). The main manifestation of actinomycosis of the central nervous system is a brain abscess. Signs depend on localization, and are determined by the rate of abscess development, the degree of displacement or destruction of brain tissue. The main symptoms are headache, increased intracranial pressure, focal symptoms, hemiparesis, aphasia, ataxia, and abnormal reflexes (Slack and Gerencser 1975).

Actinomycosis of bones and skin

Unlike some animals, bone involvement is rare in human actinomycosis (Table 1). The process is usually due to the direct spread of infection from adjacent soft tissues. This leads to periostitis, which stimulates new osteogenesis, visible on radiographs. At the onset of the disease, limited areas of bone destruction surrounded by denser bone tissue can be observed. In such cases, the mandible, ribs, and spine are most often involved. Although actinomycotic lesions of other bones have been described, they have not been confirmed by culture. Actinomycosis of the skin is extremely rare (Table 1). The source is mainly wounds contaminated with saliva or plaque, or human bites or fistfight injuries. Hematogenous spread of the pathogen into the skin may also occur. The clinical picture of cutaneous or wound actinomycosis is very similar to that of the cervicofacial form.

Epidemiology of actinomycosis

Bacteria isolated from human actinomycotic lesions essentially belong to the resident or transient innate mucosal microflora. Thus, except for actinomycosis resulting from human bites or injuries in a fistfight, the disease is always endogenous in origin and therefore not capable of either epidemic outbreaks or transmission in the usual sense.

Although sporadic actinomycosis occurs worldwide, however, the incidence of actinomycosis seems to vary from continent to continent, country to country, or even region to region, possibly reflecting changing standards of dental care and differences in the amount and types of antibiotics used. . Such factors may explain the lower absolute and relative incidence of cervicofacial actinomycosis in the US compared to Europe, but the higher prevalence of thoracic and abdominal infections in the North American continent.

Based on histological studies, Hemmes (1963) calculated the frequency of actinomycotic infections in the Netherlands: 1 per 119,000 inhabitants per year. For the region of Cologne in Germany before 1969, Lentze (1969) reported an incidence of 1 in 83,000. Subsequently, this incidence was recalculated for 1970-85. and a range of 1 in 40,000 (acute and chronic cases combined) to 1 in 80,000 (chronic cases only) per year has been defined (Schaal 1979). This is significantly higher than the incidence of actinomycosis in other areas of Germany and in other European countries. Such differences are difficult to explain, but they may be due to local differences in diagnosis rather than true epidemiological differences.

It has long been known (Slack and Gerencser 1975, Pulverer and Schaal 1978, Schaal 1981, Schaal and Beaman 1984) that typical actinomycosis occurs 2.5-3.0 times more frequently in men than in women. In addition, epidemiological data show that the unequal distribution of the disease by sex is limited only to patients of puberty. Before puberty and in menopause, actinomycosis is evenly distributed between the sexes (Pulverer and Schaal 1978, Schaal 1981). This suggests that the disease can occur in all age groups (Slack and Gerencser 1975, Pulverer and Schaal 1978, Schaal 1981). Among the observed patients, the youngest was 1.5 months old, and the oldest was 89 years old. However, the highest incidence of actinomycosis was observed in men aged 21 to 40 years and in women aged 11 to 30 years (Pulverer and Schaal 1978, Schaal 1981, 1992, Schaal and Beaman 1984).

Pathology and pathogenesis

The initial stage of an acute disease is an inflammatory process that leads to the formation of an abscess or, if the course is chronic, tissue proliferation develops and multiple small abscesses form. More advanced processes are characterized by scar tissue in the center and with granulations on the periphery, which may include multiple purulent foci or cavities with many fistulous tracts. Rarely, in cases. when bone tissue is involved, osteoclastic and osteoblastic changes may occur.

Druses of actinomycetes can be found in the purulent focus. They are found in the contents of the abscess or in the discharge from the fistulas in approximately 25% of cases, which is of great diagnostic value. Druses are up to 1 mm in diameter and are visible to the naked eye. These are yellowish (with a reddish or brownish tinge) particles, resembling cauliflower at small magnifications. Under the microscope, after slight pressure between the slide and cover slip, it can be seen that they are composed of a different number of spherical lobes, which represent filamentous actinomycotic microcolonies formed in vivo and generally form a cauliflower-type structure. The surrounding tissues are usually infiltrated with polymorphonuclear leukocytes.

Fully crushed and Gram-stained pellets at high magnification show that the material is composed of clusters of Gram-positive, intertwined, branching mycelial filaments. Stained smears may also contain a varied number of other Gram-positive and Gram-negative rods and cocci that represent the associated flora, as well as numerous white blood cells. Predominantly in tissue material, and less often in purulent discharge, it can be observed that the tips of the peripheral filaments in the granule are covered with a club-like layer of hyaline material, which can help differentiate actinomycotic drusen from similar particles of other (microbial and non-microbial) origin. It should be emphasized that the term "sulfur granules", which is quite widely used to designate actinomycotic drusen, refers only to the yellow color of the particles, and not at all to their high sulfur content.

The main natural habitat of all fermenting actinomycetes pathogenic for humans is the oral cavity of healthy adults, where they live in significant numbers. In the digestive and genital tracts, however, they seem to be present only sporadically or in low amounts. The same applies to the oral cavity of infants before teething and already edentulous adults. This may explain why cervicofacial actinomycosis is relatively less common at very young or old age.

The relatively low incidence of the disease compared with the ubiquitous occurrence of the pathogen in adults seems to be associated with the need for tissue invasion rather than a simple mucosal defect. Such conditions are more likely to depend on local tissue damage at the site of introduction than on a defect in the function of the immune system as a whole. In this regard, a prerequisite for the establishment of fermenting actinomycetes in host tissues is the presence of a negative redox potential, on which both pathogenic actinomycetes and many associated bacteria depend. Such a local decrease in oxygen potential may be caused by a violation of blood circulation due to general circulatory disorders or vascular disease, traumatic injuries with crushing of tissues or the introduction of foreign bodies, or with the necrotic ability of other simultaneously present microorganisms.

These so-called "associated microorganisms" are, as it were, the trigger mechanism of the actinomycotic process, producing local anaerobic conditions. In addition, they enhance the relatively low invasive ability of pathogenic fermenting actinomycetes by releasing aggressive enzymes such as hyaluronidases and toxins. Thus, actinomycosis is almost always a synergistic mixed infection, in which actinomycetes are a specific component, or "leading" organism, which determines the features of the clinical course and the characteristic symptoms of the disease. The composition of the accompanying microflora varies from case to case, but it is always present and often determines the initial clinical picture and some complications.

Varieties of fermenting actinomycetes that are capable of causing typical actinomycotic lesions in humans are presented in Table 2. The most common have been identified A. israelii and A.gerencseriae, but the frequency of the latter is clearly underestimated, because they began to be separated from A. israelii starting only in 1987. The third pathogen that can cause actinomycosis in humans is P. propionicum, but this species is rarely encountered. Formerly classified as "Arachnia propionica"(Schaal 1986), it has recently been transferred to the genus Propionibacterium based on 16S rRNA sequence similarity (Charfreitag, Collins and Stackebrandt 1988). It is not always easy to decide whether the other actinomycetes mentioned in Table 2 are significant pathogens or if they are simply members of a mixed bacterial flora of little importance.

Very little is known about factors that may explain the pathogenicity of actinomycosis caused by fermenting actinomycetes. However, it has long been established (Slack and Gerencser 1975) that Actinomyces spp. may form a villous layer on their surface, which may resemble hairs, and which may promote adhesion of the pathogen to host cells (Figdor and Davies 1997).

Tab. 2. Varieties of fermenting actinomycetes isolated from foci of actinomycotic lesions in humans.

Data collected at the Institute of Hygiene, University of Cologne, 1969-84, and at the Institute for Medical Microbiology and Immunology, University of Bonn, 1984-95.

*Note: Differences between A. israelii and A. gerencseriae until 1987 they were not usually produced.

The accompanying microflora in the foci of actinomycosis may consist of both aerobic and anaerobic microbes. In more than 50% of the cases studied by Schaal, the associated microorganisms consisted exclusively of anaerobes (Table 3). In other cases, both obligate (strict) anaerobes and facultative anaerobes or aerobes were found. On average, 2-4 varieties of associated bacteria were present in the focus, but in some cases up to 10 were determined.

Table 3. Aerobic microorganisms associated with fermenting actinomycetes obtained from human lesions

Among aerobic contaminants (Table 3), the most common were coagulase-negative staphylococci, Staphylococcus aureus, alpha-hemolytic and beta-hemolytic streptococci. Anaerobic and capnophilic (microaerophilic) accompanying microflora is much more diverse and numerous. Synergistic interactions likely exist between A. israelii and A. gerencseriae With Actinobacillus (Haemophilus) actinomycetemcomitans. The last microorganism, whose name refers to its characteristic resemblance to actinomycetes, is often the cause of a particularly chronic course of the disease and ineffective treatment. This pathogen can maintain an inflammatory process with similar symptoms even after chemotherapy completely eliminates actinomycetes. Other common actinomycete companions are black pigmented Bacteroidaceae (Prevotella spp., Porphyromonas spp.), unpigmented Prevotella and Bacteroides spp., Fusobacteria, the so-called microaerophilic streptococci, which belong mainly to the variety Streptococcus anginosus(milleri), propionibacteria and Eikenella corrodens(Table 4).

Table 4. Anaerobic microorganisms associated with fermenting actinomycetes obtained from human lesions

Based on Schaal and Lee (1992).

Very little is known about the humoral and cellular immune responses of patients suffering from actinomycosis. Antibodies against fermentative actinomycetes can be detected in human serum by various methods, including immunofluorescence and enzyme immunoassay. Most of these antibodies react more actively with antigens A. naeslundii and A. viscosus than with A. israelii, A. gerencseriae, or P. propionicum. In addition, antibodies are mainly associated with the presence of periodontal disease and rarely with previous or existing invasive actinomycosis. Thus, it has been established that the antibody response in actinomycosis is insignificant or sporadic. In addition, antibodies probably have no protective effect against actinomycetes, and their presence is in no way an indication of self-healing from this disease.

On the other hand, it was established long ago (Lentze 1938) that the immune system of patients with actinomycosis can be stimulated by the introduction of formalin-killed cells or extracts of cells of pathogenic actinomycetes (actinolysate). This results in an antibody response that can be measured. More importantly, however, after the introduction of actinomycotic antigens, a so-called local reaction occurs, that is, a temporary increase in inflammation. The immune response formed after repeated injections helps to overcome the disease. These observations provide the basis for the vaccine treatment of actinomycosis, which was used before antimicrobial therapy (Lentze 1938, 1969).

Diagnostics

The diagnosis of human actinomycosis is mainly based on the isolation and identification of causative agents because clinical symptoms are often misleading and histopathology and serology are low specific and low sensitive. The presence of drusen, which sometimes give the pus the appearance of semolina, should initiate a search for actinomycetes. However, given that only 25% of actinomycotic pus specimens contain these granules, their absence does not exclude the diagnosis of actinomycosis.

Collection and transportation of pathogenic material.

Suitable pathological material for bacteriological analysis of actinomycosis is pus, discharge from fistulas, bronchial secretions, granulation and biopsy specimens. During sampling, precautions should be taken against contamination by congenital mucosal microflora. Whenever possible, pus or tissue should be obtained by percutaneous puncture. To diagnose thoracic actinomycosis, bronchial secretions must be obtained transtracheally. Sputum examination is unreliable because it usually contains oral actinomycetes, including pathogenic varieties. Transthoracic percutaneous needle biopsy or percutaneous needle aspiration of suspicious abdominal abscesses is often the only means of obtaining satisfactory specimens for diagnosis. Transportation of specimens to the bacteriological laboratory should be reasonably quick. If long-term transport is unavoidable, special transport media such as Stewart's must be used, although fermentative actinomycetes are less susceptible to oxidative damage than strict anaerobes.

microscopic examination

When drusen are present, this makes it possible to quickly and relatively reliably make a preliminary diagnosis after examination at low magnification (d 100) of an actinomycotic granule placed under a coverslip and with a drop of 1% solution of methylene blue. Actinomycotic drusen appear as cauliflower-like particles with an unstained center and a blue periphery, in which leukocytes and short filaments, sometimes with clubs, radiate from the center of the granule. Gram-stained smears obtained by squeezing pellets between two slides show filamentous, branching, Gram-positive structures that represent pathogenic actinomycetes, as well as a variety of other Gram-negative and Gram-positive bacteria that indicate the presence of concomitant microorganisms. The presence of these bacteria is necessary to distinguish actinomycotic drusen from granules formed by various aerobic actinomycetes ( Nocardia, Actinomadura, Streptomyces), which never contain accompanying microflora. Direct and indirect immunofluorescence for the detection of specific antibodies can also be used to identify actinomycete species present in the granule without culture isolation.

Cultural diagnostics

To obtain reliable results, it is advisable to use transparent media so that the plates can be carefully examined for the characteristic filamentous colonies, and cultured for at least 14 days. Cultures can be examined every 2-3 days without altering anaerobic conditions if the method of Fortner (1928) is used to obtain a low oxygen potential. If anaerobic flasks or plates are used, it is advisable to inoculate two or three media at the same time to examine them for actinomycete growth after 3, 7 and 14 days. Since the removal of plates from an anaerobic environment usually stops the further growth of microorganisms that need a long incubation without changing the anaerobic conditions.

Preliminary culture results are obtained after 2-3 days, when characteristic arachnid microcolonies can be seen under a microscope. A. israelii, A. gerencseriae or P. propionicum. Confirmation of preliminary microscopic or early culture diagnoses by unambiguous identification of the pathogenic variety of actinomycetes can take 14 days or more. This is necessary to reliably identify the differences between fermenting actinomycetes and morphologically similar contaminants obtained from the mucous membranes of the patient, as well as similar aerobic actinomycetes of the genera Nocardia, Actinomadura and Streptomyces. A detailed bacteriological analysis of the associated microflora may also be helpful in selecting appropriate antibiotic therapy.

Molecular methods, such as genetic studies or polymerase chain reactions (PCR), are currently being developed and may in the future be able to allow faster diagnosis of actinomycosis.

Serological diagnosis.

Actinomycotic infection does not necessarily stimulate a humoral immune response, which can be detected by available laboratory methods. However, none of the methods used, with a wide variety of antigens used, did not provide satisfactory results due to problems with sensitivity and specificity (Holmberg, Nord and Wadström 1975, Holmberg 1981, Persson and Holmberg 1985).

Treatment

Surgical dissection of actinomycotic foci and drainage of purulent contents is always the basis for the treatment of actinomycosis. However, it is known that even a radical operation often only ends with a temporary reduction in symptoms and may be accompanied by one or more relapses. In order to overcome these problems, in the past they tried to use substances such as iodides, thymol, copper sulfate, hydrogen peroxide, silver nitrate, arsenic preparations, which, however, did not improve long-term results. Only subcutaneous injection of killed cells of actinomycetes (heterovaccine Lentze 1938) showed some effectiveness.

Progress in the treatment of actinomycosis appeared when sulfonamides and penicillin became available. Penicillin was active against pathogenic actinomycetes in vitro and in vivo. Given that in many patients the effect of penicillin therapy was insufficient or absent, treatment with large doses of penicillin was often recommended for at least 3 months and up to 12-18 months (Harvey, Cantrell and Fisher 1957).

A poor response to penicillin treatment is often due to the presence of concomitant bacteria that are penicillin-resistant. In addition, drugs do not penetrate well through the dense tissue of actinomycotic burns and into drusen. Finally, A. actinomycetemcomitans- usually resistant to penicillin, although they do not produce beta-lactamase. Thus, penicillin in the treatment of actinomycosis is effective only when it is not present. A. actinomycetemcomitans and when the accompanying microflora does not contain any beta-lactamase producers.

Aminopenicillins are somewhat more active against pathogenic actinomycetes than penicillin, and, in addition, they inhibit growth A. actinomycetemcomitans. However, given that they are not resistant to the action of beta-lactamases, the microorganisms that produce beta-lactamases may interfere with their therapeutic efficacy. This rarely occurs in cervicofacial actinomycosis, but beta-lactamase producers are usually present in thoracic and especially abdominal infections. Therefore, currently used treatment regimens include drugs that are effective against actinomycetes and the potential producers of beta-lactamase type S. aureus, gram-negative anaerobes, and, in cases of abdominal actinomycosis, Enterobacteriaceae.

The current recommendations for antibiotic therapy for actinomycosis are as follows: The therapy of choice for cervicofacial actinomycosis is amoxicillin plus clavulanic acid or possibly ampicillin plus sulbactam. The initial dose is 2 g 3 times a day of amoxicillin plus 0.2 g 3 times a day of clavulanic acid per day for 1 week, and 1 g 3 times a day of amoxicillin plus 0.1 g 3 times a day of clavulanic acid per day for another week. In rare cases, chronic infections of the cervicofacial region may require up to 4 weeks of treatment. The indicated treatment regimen can also be used for thoracic actinomycosis, but in these cases it is recommended to give a high dose for a longer time - for 3-4 weeks. In long-term chronic cases of pulmonary actinomycosis, an increased dose of ampicillin may be necessary to increase tissue concentration. Depending on the associated flora, aminoglycosides may also be needed, especially when there is a persistent presence Enterobacteriaceae type Klebsiella spp. or Enterobacter spp. The latter are generally usually present in abdominal actinomycosis. The therapy of choice for these infections is a combination of amoxicillin and clavulanic acid with metronidazole (or clindamycin) for severe anaerobes plus tobramycin or gentamicin. Imipenem may be a suitable alternative, but it has been rarely used to treat actinomycotic infections (Edelmann et al. 1987, Yew et al. 1999).

It is important to note that neither metronidazole nor clindamycin can be used to treat actinomycotic infection alone without added antimicrobial agents, especially aminopenicillins, because clindamycin is almost ineffective against A. actinomycetemcomitans(Niederau et al. 1982, Schaal 1983, Schaal et al. 1984) and metronidazole is inactive against pathogenic actinomycetes (Schaal and Pape 1980, Niederau et al. 1982). Tetracyclines or cephalosporins can be used instead of aminopenicillins for the treatment of penicillin-allergic patients, but the clinical efficacy of these drugs is much less than that of aminopenicillins or the combination of aminopenicillins with beta-lactamase inhibitors.

Forecast

Before the appearance of modern antibiotics in practice, the prognosis of actinomycosis was doubtful - closer to unfavorable. Even today, patients receiving inadequate therapy can suffer from actinomycosis for many years and even die from the disease or its complications. This is especially true for thoracic and abdominal infections, which are often diagnosed only in the last stage. If the diagnosis is established early and antibiotic therapy is adequate, then the prognosis of cervicofacial and cutaneous actinomycosis is generally good. Thoracic, abdominal and systemic manifestations, however, remain a serious problem and require active management.

Other diseases caused by fermenting actinomycetes

Fermenting actinomycetes can also cause some other diseases, but they differ significantly from typical actinomycotic lesions in clinical manifestations, prognosis, and treatment; therefore, they should not go under the term actinomycosis. However, some of them are no less important than actinomycosis, both from a medical and economic point of view.

Canaliculitis and other eye infections

The most common disease not associated with trauma and caused by fermenting actinomycetes is lacrimal canaliculitis with and without conjunctivitis. This disease is usually characterized by yellowish to brownish growths within the tubule and pus in the inner corner of the eye. The most important causative actinomycetes are P. propionicum, A. viscosus and A. israelii(Table 2). Less frequently isolated A. naeslundii, A. gerencseriae and Actinomyces odontolyticus(Schaal and Lee 1992). Associated bacteria are often present, but not always. Excluding availability Streptococcus pneumoniae or haemophilus influenzae in the eyes and A. actinomycetemcomitans in the cervicofacial form of actinomycosis, the accompanying flora in both lesions is very similar.

In addition to lacrimal canaliculitis, ocular infections caused by fermenting actinomycetes can also present as conjunctivitis, keratitis, dacryocystitis, inflammation of the mucosal glands of the eyelid, and even periorbital abscess, granuloma, or intraocular infection (Schaal 1986, Schaal and Lee 1992). A reliable diagnosis of lacrimal canaliculitis and other actinomycotic ocular lesions is made in accordance with the bacteriological procedures mentioned above. Removal of tear adhesions that are commonly found in canaliculitis and topical antibiotics almost always result in a quick cure in cases where there is a non-invasive process. Invasive infections (abscesses, granulomas, intraocular infections) require systemic therapy with appropriate antibacterial drugs.

Conditions associated with intrauterine contraceptives (IUDs).

As discussed earlier in the section on abdominal actinomycosis, the uterus and cervix of women in the presence of intrauterine contraceptives or vaginal fallopian rings are often colonized by a complex bacterial flora that consists of enzymatic actinomycetes and various other aerobic and anaerobic bacteria (Eibach et al. 1989, Schaal et al. Lee 1992). These organisms are particularly abundant directly on the IUD threads within the cervical canal, and closely resemble the characteristic polymicrobial flora of actinomycotic lesions. The predominant actinomycetes under these circumstances are A. Israelii. Relatively often found A. viscosus. Other varieties were also sometimes isolated (Table 2). The associated flora in these cases is very similar, but not identical, to cervicofacial actinomycosis (see Tables 3 and 4). Of the aerobic bacteria in the IUD, enterococci are more or less often found, Enterobacteriaceae and Gardnerella vaginalis(Table 3). Although anaerobes and capnophiles (microaerophiles) are commonly present (Table 4), a much lower frequency of isolation should be noted. A. actinomycetemcomitans and an even lower incidence of Fusobacteria in IUD than in cervicofacial actinomycosis, whereas unpigmented varieties Bacteroides and Prevotella, E. corrodens and lactobacilli are more commonly isolated from IUDs. The presence of fermenting actinomycetes and characteristic associated bacteria on the ICH and in the cervical canal is not necessarily associated with symptoms of an aggressive actinomycotic infection that requires specific treatment. However, approximately 28% of patients with actinomycetes in the cervix or IUD had symptoms of lower genital tract infection, and another 26% had upper genital tract infection (Eibach et al. 1989, 1992). Symptoms such as fever, pain, or vaginal discharge usually resolve within 4 to 8 weeks after removal of the IUD, at least for lower genital tract infections.

When typical actinomycetes are found on the IUD or in the cervical canal, the use of the IUD should be discontinued. After the return of the microflora to normal levels, the IUD can be used again without increasing the risk of developing actinomycosis of the genital organs.

Other suppurative infections

Fermenting actinomycetes can also cause other inflammatory processes. These include pharyngitis, otitis media, urethritis, funicitis (inflammation of the umbilical cord) (Wright et al. 1994), cutaneous and subcutaneous purulent lesions, abscesses with or without associated mixed anaerobic flora, empyema, and septicemia (Schaal 1986).

These infections can cause not only "classic" Actinomyces spp., type A. naeslundii, A. viscosus, A. odontolyticus and Actinomyces meyeri, but also some others Actinomyces spp. and Arcanobacterium haemolyticum, such as: Actinomyces pyogenes, Actinomyces neuii subsp . neuii, Actinomyces neuii subsp . anitratus(Funke et al. 1994), Actinomyces bernardiae(Funke et al. 1995), Actinomyces radingae, Actinomyces turicensis(Wmst et al. 1995), Actinomyces europaeus(Funke et al. 1997) and Acinomyces graevenitzii(Ramos et al. 1997). It has also been described as a new actinomycete-like variety Acinobaculum schaalii(Lawson et al. 1997), which was isolated from patients.

Diseases caused by aerobic actinomycetes

Aerobic actinomycetes with an oxidative type of carbohydrate metabolism constitute a large and very heterogeneous group of filamentous bacteria, which have recently been divided into subsections. Micrococcineae, Corynebacterineae, Micromonosporineae, Pseudonocardineae, Streptomycineae, Streptosporangineae, Frankineae and Glycomycineae order Actinomycetales within a newly defined class Actinobacteria(Stackebrandt, Rainey and Ward - Rainey 1997). They are widely distributed in nature, especially in the soil, and many play a significant role in the turnover of organic remains. Only a few of these microorganisms are of medical importance as infectious agents or as sources of strong allergens. They belong to families Cellulomonadaceae, Dermatophilaceae, Nocardiaceae, Gordoniaceae, Tsukamurellaceae, Pseudonocardiaceae, Streptomycetaceae, Nocardiopsaceae and Thermomonosporaceae. Depending on the actinomycete species involved, its location and mechanism of introduction, and host immune status, aerobic actinomycetes can cause a variety of diseases in humans and animals. In addition, once it has been established, these organisms can cause nosocomial infections, such as catheter-related sepsis or postoperative wound infections. The most common pathogens responsible for these diseases belong to the genera Nocardia and Actinomadura, but other actinomycetes of the type Amycolatopsis, Gordonia, Nocardiopsis, Pseudonocardia, Rhodococcus, Saccharothrix, Streptomyces and Tsukamurella(Schaal and Lee 1992, McNeil and Brown 1994).

An infectious disease caused by radiant fungi (actinomycetes) and having a primary chronic course with the formation of dense granulomas, fistulas and abscesses. Actinomycosis can affect not only the skin, but also internal organs. Diagnosis of the disease is based on the detection of the characteristic mycelium of fungi in the discharge and the detection of the growth of specific colonies when sown on nutrient media. In the treatment of actinomycosis, the administration of actinolysate is used in combination with antibiotic therapy, ultraviolet radiation of the skin, and iodine electrophoresis. According to indications, abscesses are opened, surgical treatment of fistulas, drainage of the abdominal and pleural cavities is performed.

Forecast and prevention of actinomycosis

In the absence of specific treatment, actinomycosis of internal organs can lead to death. The mildest form is considered to be cervico-maxillofacial actinomycosis. After recovery, patients may develop relapses.

There is no specific prevention of actinomycosis. Nonspecific prevention includes hygiene, prevention of skin injury, timely dental treatment, inflammatory diseases of the oral cavity, tonsils, respiratory organs and gastrointestinal tract.

Actinomycosis of the skin and subcutaneous tissue is a purulent chronic (very rarely, acute) disease that lasts for years, affecting people, mainly at working age, and tending to progress in the absence of adequate therapy. Among skin purulent diseases with a chronic course, it accounts for 3 to 5%.

The main signs of actinomycosis are the formation of specific granulomas and a chronic inflammatory process, which occur with suppuration due to the addition of a secondary bacterial infection (up to 80% of cases), the development of abscesses and phlegmon, the further formation of fistulas with the presence of purulent discharge from them. The disease can cause intoxication of the whole organism, disruption of the functioning of the affected organs, lead to the development of chronic anemia and amyloidosis.

What are the causes of actinomycosis?

On the body and in the human body there is a huge number of different microorganisms - viruses, bacteria, fungi, protozoa. They make up the normal microflora, which under normal conditions does not harm him in any way. Very often it is impossible to draw a line between pathogenic microorganisms and saprophytes included in this composition. This is due to the fact that all these microorganisms can be, depending on the conditions, both completely harmless and become the cause of the infectious process.

For example, even lactobacilli and bifidobacteria, which are completely harmless and necessary for the body, can cause a pathological condition with a significant degree of colonization. At the same time, such pathogenic microorganisms as meningococci, pneumococci, clostridia, existing on the surface of the skin and on the mucous membranes of a person, are not able to cause an infectious disease, due to the protective properties of the body and the high competitive ability of the microflora that was formed earlier.

About the pathogen

One of these infectious agents with "double" properties are actinomycetes, or "radiant fungi", which are involved in the formation of a set of microorganisms (microflora) that exist in symbiosis (under certain conditions) on the body and in the body. They are characterized by a wide distribution in the environment - on plants, in mineral and spring water sources, in tap water, on the soil surface, etc. and are a group of facultative gram-positive anaerobic bacteria capable of forming well-developed branching "threads" at certain stages of development. » (mycelium).

As saprophytes in the human body, they are found on the skin, on the mucous membrane of the oral cavity, gums, bronchi, upper respiratory tract, stomach and intestines, folds (lacunae) of the tonsils, vagina, in the cavity of teeth affected by caries, in plaque and teeth. -gingival pockets, anal folds, etc.

Thus, the causative agent of actinomycosis is not one type of actinomycetes. The disease is most often able to cause bacteria such as Actinomyces israelii, A. albus, A. bovis, A. candidus, A. violaceus, Micromonospora monospora, N. Brasiliensis. In recent years, the number of detected actinomycetes as pathogenic has been increasing more and more. In the specialized literature, there are more and more articles describing actinomycosis caused by such rare species of bacteria as A. viscosus, A. turicensis, A. meyeri, Propionibactericum propionicus, A. radingae, A. graevenitzii and many others.

Is actinomycosis contagious or not?

Despite the fact that actinomycosis is an infectious pathology, at the same time, this disease is non-contagious, that is, sick people and animals are not contagious. The activation of actinomycetes is facilitated by such provoking factors as weakening the body's immune defenses, physical and psychological overwork, various chronic diseases of internal organs (diabetes mellitus, peptic ulcer, hemorrhoids, chronic cholecystitis, etc.), skin and chronic foci of infection.

Radiant mushrooms actinomycetes

Disease pathogenesis

Actinomycetes and their accompanying bacteria can enter the body in an exogenous way, in which damaged skin and mucous membranes serve as the entrance "gate", or endogenously - by contact, hematogenous (very rarely), lymphogenous way.

As a rule, the development of actinomycosis is preceded by a traumatic injury of a different nature, for example, bruises and fractures, as well as abrasions and diaper rash, the use of intrauterine contraceptives, traumatic tooth extraction, cracks in the anus, sacrococcygeal cyst, hidradenitis, etc. .

In the process of emergence and the further mechanism of development, the accompanying anaerobic and aerobic microorganisms that secrete hyaluronidase and other enzymes that melt the connective tissue structures, which contribute to the spread of the actinomycosis process, are of no small importance. In most cases, the mechanism for the development of pathology is due to the multiple microbial flora - a combination of actinomycetes with staphylococci, streptococci, fusobacteria, enterobacteria, bacteroids, etc. In relation to the local manifestations of the disease, 3 stages of its development are distinguished:

1. The infiltrative stage, which is the gradual formation of a specific granuloma, which is called actinomycoma. It consists of a capsule, inside which there are leukocytes and giant cells, infiltrative tissue, microscopic abscesses, granulations and proliferative elements, connective tissue bridges. This stage proceeds without special subjective sensations and visible clinical symptoms.
2. The stage of abscessing is the formation of larger abscesses from microabscesses in granuloma tissue, often with an abundant content of drusen.
3. Fistulous stage - rupture of the capsule and opening of abscesses with the formation of one or multiple mouths of fistulous passages.

The rate of spread of the process is influenced by various factors, for example, the degree of immune defense of the body, age, localization of the focus, the timeliness and adequacy of treatment, and many others.

Pathological changes in actinomycosis and histological characteristics of the focus

A characteristic macroscopic picture is the formation of granulomas (nodules) with their further destruction and suppuration. In parallel with these processes, fibrosis occurs in festering granulomas, followed by the development of scar tissue, which resembles cartilage in its density. This tissue, due to the formation of multiple microabscesses in it, has a spongy structure that resembles a honeycomb.

Microscopically, the pathomorphological picture is characterized by a proliferative reaction around the pathogen that has penetrated into the tissue and the formation of a granuloma. The latter delimits the emerging focus of infection from the surrounding healthy tissues. Histology of actinomycosis (with microscopic examination) reveals a change in the cellular composition of the granulomatous formation at different stages of its development. It is expressed by a necrotic process and cellular decay in the central sections of the granuloma and the formation of a fibrous structure around the granulation tissue.

Typical for granulomas in actinomycosis are fibrotic processes, the severity of which depends on the degree of reaction of a particular organism, and yellowish clusters formed by xanthomic cells. The latter are multinuclear or mononuclear phagocytes located in the dermis and hypodermis, having a foamy cytoplasm, which contains fatty inclusions. Also characteristic is a certain inversely proportional pattern of the relationship of xanthomous cells with bacterial colonies - with a small number of filaments of actinomycetes, there are many xanthomous cells, and vice versa.

In the histological structure of granulomas in actinomycosis, two types (stages) of structure are distinguished:

1. Destructive - the first option, or the initial stage. Characteristic for the histological picture of this stage is the presence of granulations, which contain polymorphonuclear leukocytes. Granulation tissue consists of young (mainly) connective tissue cells, prone to suppuration and the process of decay.
2. Destructive-productive - the second option, or the second stage. Histological sections under the microscope are characterized by the diversity of the composition of the granulation tissue. In addition to the cells listed above, lymphoid, xanthoma, epithelioid and plasma cells, large hyaline spots ("hyaline balls") and collagen fibers are also found. In addition, microabscesses of various sizes and hyalinized scars are revealed.

Along with the variants of tissue reaction described above, of great importance for the diagnosis of the disease under consideration is the histological detection of actinomycete drusen of different sizes, which are plexuses of thin filaments of an uneven, usually lobular structure, arranged radially. Sometimes they look like sticks, but more often at their ends a thickening in the form of a flask is determined. It is assumed that these swellings are not detected in the clinically severe course of the disease.

Drusen are tissue colonies of actinomycete bacteria. The main role in their formation is played by the body's immune response in response to antigens that secrete pathogens into the surrounding tissues. Thus, the formation of drusen is a protective reaction of the macroorganism, which results in a slowdown in the spread of the pathogen and the process of localization of the developing pathological process.

A collection of filaments (drusen) surrounded by a collection of leukocytes and epithelioid cells, around which there may be giant cells, is usually noted in the central section of the granuloma. During the histological examination, simultaneously with the identification of drusen, their condition is necessarily assessed, which is determined by the reaction of the surrounding tissues to them. In this regard, there are 4 groups of changes that can occur with drusen:

• their marginal or total dissolution (lysis);
• calcification, that is, the deposition of calcium salts in them (calcification);
• absorption by giant cells (phagocytosis);
• transformation into a glassy amorphous mass.

The first and third types of changes (lysis and phagocytosis) characterize an increase in the degree of the body's immune defense. Of particular importance is the comparison of the histological pattern of tissue response and changes in the state of drusen to assess the effectiveness of the methods of therapy and drugs used.

The detection of typical actinomycotic drusen during histological examination is a reliable sign of the disease. At the same time, the formation of drusen is not characteristic of all varieties of the pathogen. For example, they do not form with nocardiosis. Therefore, their absence, especially at the initial stage of the diagnosis, is not yet proof of the absence of the disease.

In this regard, in some cases, the diagnosis of actinomycosis should be based not only on the assessment of pathomorphological data and the histological picture, but also on microbiological examination. The latter consists in microscopic examination and inoculation of the necessary material on various nutrient media. In this case, the optimal temperature for growing the alleged pathogen is body temperature (35 ° -37 °). Grown cultures are subsequently stained with methylene blue or Gram and examined under a microscope. They are determined by the threads or rods of actinomycetes with cone-shaped ends or staining like a rosary.

Symptoms

The incubation period of actinomycosis can range from 2-3 weeks to several years, and the course of the disease can sometimes be acute, but most often it is initially chronic. Skin lesions can be:

1. Secondary.
2. Primary.

Secondary cutaneous actinomycosis

The vast majority of cases of this skin pathology develops a second time as a result of the spread of the pathogen from the main lesion. At the same time, the appearance in the skin of a bumpy, slightly painful cyanotic-purple infiltrate is noted. A characteristic feature of the actinomycotic infiltrate is its woody density and the absence of clear outlines.

In some places, it sometimes defines areas of softening and openings of thin fistulous passages, through which purulent-bloody contents that are odorless are released. Fistulous secretions often contain drusen. Sometimes you can see granules with a diameter of about 2 - 3 mm, white or yellowish. The mouths of the fistulous passages most often look like points raised above the level of the skin, but may be retracted or with granulations.

When localized in the neck, inguinal or axillary region, skin folds are formed in the form of rollers, and the skin acquires a purple-cyanotic color. Very often, such changes are preceded by chronic purulent. The area of ​​the focus is slightly painful or painless. The process itself sometimes resembles chronic, phlegmon or coccidioidomycosis. The defeat of regional lymph nodes is rare, and the nature of the primary lesion affects the subjective sensations.

Primary actinomycosis of the skin

The primary skin lesion first manifests itself, as in the previous case, with one or more limited, painless, dense nodules located in the hypodermis. In the future, they increase and, merging with each other, turn into one infiltrated plaque with a woody density. At the same time, the skin in the lesion acquires a bluish-red color.

Gradually, in one, and sometimes simultaneously in several areas of the infiltrate, its softening occurs. The skin in these places becomes thinner and spontaneously opens with the formation of fistulas, from which purulent-bloody or purulent contents of a yellowish color are released. Subjective sensations in the primary skin lesion are insignificant or absent.

Pathology can have, practically, any localization, moreover, numerous. Foci can be located both on the body (head and neck region, chest and mammary glands, axillary and inguinal zones, abdominal wall, buttocks, perineum and pararectal zone, limbs) and in the ENT organs, and in the internal organs - lungs, genitals, liver and intestines, especially the caecum and rectum.

Lesions in actinomycosis of the skin

cervicofacial form

Depending on the localization of the foci, various clinical forms of the disease are distinguished, for example, actinomycosis thoracic, abdominal, etc. The most common clinical form is actinomycosis of the maxillofacial region. It is detected in 5-6% of patients who go to medical institutions about purulent-inflammatory processes in this zone and in approximately 58% of people suffering from this pathology.

This form of the disease proceeds relatively (compared to other forms) favorably. At the same time, the associated secondary purulent infection has a significant effect on its course and clinical symptoms. This contributes to a change in the nature of the course of the process and to multiple exacerbations.

Depending on the severity and predominant localization of the process, the following main clinical forms of actinomycosis of the maxillofacial region are distinguished:

Skin

It occurs quite rarely. The usual localization of the pathological focus is the buccal, submandibular and chin areas. It appears on the skin as pustules, tubercles, or a combination of them. These elements create small separate or confluent infiltrates of a spherical or hemispherical shape that rise above the surrounding healthy areas. Often there is a spread of the process to healthy areas.

Subcutaneous

Also a relatively rare form. It is characterized by the appearance of a limited infiltrate in the subcutaneous adipose tissue. The infiltrate is located directly in the zone of the tissue site, which is the entrance "gateway" for the pathogen. The most common localization is the area of ​​the cheeks, corresponding to the level of the upper or lower jaw, at the level or under the lower jaw. In some cases, the development of a focus with a predominance of edema is noted, in others - a proliferative process. With this form, the spread of the main focus along its length with the formation of new foci is possible.

Subcutaneous, intermuscular, or deep

The predominant localization of the actinomycotic process is under the fascia that covers the chewing muscle (mainly in the projection of the angle of the lower jaw). The clinical picture is characterized by great diversity. Usually edema appears, followed by soft tissue hardening, facial asymmetry. Somewhat less often, the focus is formed in the parotid and temporal regions, in the zone of the pterygo-jaw space, the fossa behind the lower jaw.

With these localizations, muscle spasm (trismus) of varying degrees often develops, which is one of the first signs of the disease. The sluggish process can last even several months, after which pain and high fever appear, accompanying the formation of abscesses and softening of the infiltrate, the formation of fistulas, from which purulent or purulent-bloody contents are released, sometimes with yellow grains (druze).

Also characteristic is a long-lasting bluish color of the skin around the fistulous openings. After that, it is possible to resolve the process or form new foci up to the involvement of bone tissues. It is this form of the disease that is often accompanied by the addition of a purulent infection, as a result of which the process proceeds sharply, rapidly and spreads along the length. The focus of actinomycosis very rarely can spread not only to the buccal areas, but also to the lips, tonsils, larynx and trachea, eye sockets. However, its course, in comparison with other forms, is relatively favorable.

Cervical-facial form of the disease

Diagnosis and principles of treatment

Diagnosis is not associated with any difficulties in cases of a detailed typical clinical picture. The initial stages of the disease are much more difficult to diagnose. A certain importance in the diagnosis is given to an intradermal test using actinolysate, however, only positive and sharply positive reactions are taken into account, since a weakly positive test can be in other diseases, and a negative one is not a reason to exclude the disease, since it can be such and with immunosuppression. In 80% of cases, the reaction of binding a compliment with actinolysate is positive. The most reliable values ​​are the detection of actinomycetes in pus secreted from fistulas, in tissue biopsy, in druses, including with the help of inoculation of materials on a nutrient medium (cultural diagnostics), x-ray, histological (microscopic) studies.

Differential Diagnosis

It is carried out mainly with lupus, collicative (scrofuloderma), with abscesses caused by a common purulent infection, with benign and malignant neoplasms.

Therapy

Due to the peculiarities of the causative agent of the disease, the mechanisms of its development and the variety of clinical manifestations, the treatment of actinomycosis should be comprehensive, including:

• the use of anti-inflammatory drugs, including antibiotics, taking into account the sensitivity of the accompanying microflora to them;
• conducting immunomodulatory therapy with actinolysate;
• the use of general strengthening drugs;
• physiotherapeutic effect (iodine phonophoresis, UHF and UVI, etc.).

If necessary, surgical treatment is carried out, the meaning of which is to excise the foci, in full or partial curettage of fistulous passages, etc. The cure of the disease does not exclude its recurrence.

Photo: actinomycosis of the maxillofacial region

Actinomycosis of the skin is an infectious disease. Find out what are the causes of the disease and what effective methods of diagnosis and treatment exist.

Actinomycosis of the skin is an infectious disease caused by specific microorganisms, actinomycetes. They simultaneously possess the properties of fungi and bacteria.

When the disease develops, granulomas form in the tissues - small growths in the form of nodules. A characteristic sign of actinomycosis is suppuration of granulomas.

Skin lesions cause severe inconvenience to a sick person, pain is aggravated by rubbing inflammation on clothing.

Actinomycosis of the scalp makes hair care and combing painful. Actinomycosis of the face causes aesthetic harm to a person's appearance.

Outwardly, actinomycosis of the skin looks like multiple purulent lesions of the skin. When the granulomas break through, small yellow grains can be seen in their contents. These are drusen, or colonies of actinomycetes.

The causative agent of actinomycosis

Actinomycetes are specific microorganisms. According to the classification, they are considered bacteria, but at some stages of development in actinomycetes, mycelium is present in the structure.

Mycelium is a fungal structure that looks like thin threads. It is involved in the process of reproduction of fungi and actinomycetes.

The inflammatory process in the skin is caused by several types of actinomycetes. Some of them require oxygen, others live and reproduce only in its absence.

Actinomycetes are ubiquitous, they can be found in the soil, water bodies, dry grasses. Normally, they can be present in the human body and not cause disease.

Causes and ways of development of actinomycosis

When the disease develops, it is difficult to determine what exactly caused the infection. Scientists have long believed that the disease can develop only when actinomycetes enter from the external environment.

Later it became known that these microorganisms are often present in the composition of the normal human microflora. This is how the theory of endogenous infection, or self-infection with actinomycosis, appeared.

Actinomycetes can enter the body in the following ways:

• Air-dust way - by inhalation of dust suspensions containing a microorganism;
• Airborne - by inhalation of water suspensions;
• Contact-household - when the pathogen enters the skin or mucous membranes.

Actinomycosis of the skin is not considered a contagious disease; contact with sick people is not dangerous in itself. The leading role in the development of the disease is played by a decrease in the level of the body's defenses.

Microorganisms with such properties are called opportunistic pathogens. If a person is healthy, his immunity does not allow actinomycetes to multiply. When there are few of these bacteria in the body, they do not cause disease.

Violation of immunity, the body's natural defenses, can develop for the following reasons:

• Infection;
• Exacerbation of chronic diseases;
• Immunodeficiencies, including HIV infection;
• Drug addiction and alcoholism;
• Childhood and old age.

In childhood, immunity is not yet sufficiently formed, so the child is vulnerable to infections. The protective forces of the elderly are reduced due to a general deterioration in health.

The peak incidence occurs in the autumn-winter period, when the number of colds increases.

How to recognize actinomycosis of the skin?

The disease can be suspected when symptoms such as:

1. The formation of multiple dense painless nodules under the skin;
2. Bluish-purple coloration of the skin over the nodules;
3. Suppuration of the skin with severe pain syndrome;
4. Detection in the purulent contents of small yellow granules;
5. Fever, general malaise and weakness.

The combination of these signs is the basis for examination for cutaneous actinomycosis.

Types and stages of cutaneous actinomycosis

Actinomycosis of the skin in humans can occur in 4 forms:

1. Atheromatous - with it, seals resemble wen;
2. Tuberculous-pustular - tubercles with this form of flow have a cavity inside filled with purulent contents;
3. Gummy-nodular - with it, the tubercles have a dense, hard texture;
4. Ulcerative - this form of the disease ends with necrosis, the death of the affected tissues.

During actinomycosis, several stages can be conditionally distinguished:

If the disease is not treated, the consequence of the third stage may be tissue necrosis and the formation of a deep non-healing ulcer.

Diagnosis of actinomycosis of the skin

A visual examination of the patient's skin is often enough for a doctor to make a diagnosis.

To confirm the preliminary conclusion, experts prescribe a study of the contents of the abscesses. If the formation has not yet broken through, the doctor can perform a puncture - pierce the skin with a needle and pump out the contents of the pustule.

The easiest way to confirm the diagnosis is microscopic examination. The material for analysis is placed on a glass slide, stained and examined under a microscope. If it is possible to detect colonies of actinomycetes, drusen, additional analyzes are not required.

However, in 75% of cases, druze is not found in the content. Then diagnostic culture is most effective.

The material for analysis is placed on a special nutrient medium that ensures optimal growth of actinomycetes.

The disadvantage of such an analysis is its long-term duration - it can take up to 2 weeks before the results are obtained. But this method makes it possible to simultaneously test the effect of antibiotics on actinomycetes. In this way, the optimal treatment regimen can be selected for the patient.

Also effective are RIF (immunofluorescence reaction) and RSK (complement fixation reaction) with actinolysate. These tests give a positive result in 98% of patients with actinomycosis.

During the course of treatment, repeated studies may be necessary. Analyzes in this case are aimed at confirming the effectiveness of the chosen therapy.

Actinomycosis: drugs for therapy

The treatment of actinomycosis is carried out by a dermatologist - a specialist in skin pathologies.

Actinomycosis in humans requires an integrated approach to treatment. For effective therapy, the following methods are used:

• The use of antibiotics;
• Immunotherapy;
• Restorative therapy.

Antibiotics can inhibit the growth and reproduction of bacteria. Some species have a bactericidal effect, that is, they destroy microorganisms. This effect is achieved by the fact that antibiotics interfere with the normal respiration of the cell and its nutrition.

Antibiotics for actinomycosis are the main method of combating the disease. For the treatment of actinomycosis of the skin, penicillin preparations, tetracyclines and macrolides are prescribed.

The optimal drug is selected taking into account the data of cultural inoculation with an antibacterial test

The average duration of antibiotic therapy is 6 weeks, high dosages of drugs are used.

To prevent microflora disorders due to the use of antibiotics, their action is corrected. For this purpose, antifungal and bacterial drugs are used.

Actinolysate is a drug that increases the body's ability to fight actinomycetes. The drug is administered as an intramuscular injection.
Injections are given 2 times a week for 10-12 weeks.

The general strengthening of the body contributes to the intake of vitamin preparations.

Surgical and physiotherapeutic treatment of actinomycosis

For extensive and deep skin lesions, surgical treatment may be recommended. Excision and drainage of purulent foci facilitates the patient's condition and prevents the development of complications.

Surgical treatment of actinomycosis of the maxillofacial region may also include the removal of lymph nodes affected by actinomycetes.

Physiotherapeutic methods are aimed at the destruction of actinomycetes on the surface of the skin and in its thickness. For such treatment, phonophoresis with iodine, ultraviolet radiation and UHF (exposure to electromagnetic fields) are prescribed. In addition to the antiseptic effect, physiotherapy promotes the renewal and growth of healthy skin cells.

Price of the question: how much does the treatment of actinomycosis cost?

When treating actinomycosis in public clinics under the compulsory medical insurance policy, the patient pays only for medicines. Doctors' consultations, tests and additional examinations are free of charge.

The price of complex therapy and supervision in private medical institutions depends on the frequency of visits to the doctor. In addition, the cost of therapy is affected by the volume of prescribed examinations and procedures.

In general, such treatment may require about 10,000-20,000 rubles.

Treatment of actinomycosis folk remedies

When actinomycosis develops, folk remedies can only act as adjuvant therapy. Relying only on traditional medicine recipes is too dangerous.

For general strengthening of the body and increasing immunity, tinctures of medicinal herbs are used: eleutherococcus, aralia, calendula. Reception of such funds should be coordinated with the attending physician. Alcohol-containing solutions may reduce the effectiveness of antibiotics.

Externally, the following agents are applied to the affected areas:

• Alcohol tincture of garlic, diluted with distilled water;
• Freshly squeezed onion juice in the form of lotions;
• Tincture of calendula flowers (used for washing and lotions).

Possible complications of actinomycosis

Actinomycosis of the skin is a disease that, without treatment, has an unfavorable prognosis.

The most common complication is the development of abscesses - extensive areas of purulent inflammation. Abscesses require surgery and do not heal well. After their resolution, visible scars remain on the skin.

The cutaneous form of actinomycosis can lead to damage by actinomycetes of other organs and tissues. Most often, the bones that are located close to the affected area of ​​​​the skin are affected. Maxillofacial actinomycosis can spread to the jaw bones and teeth.

The lymphatic system of the head and face has a special structure. Inflammation in this area can lead to infection of the brain and its membranes.

The most common complication is the development of abscesses - extensive areas of purulent inflammation

Prevention of actinomycosis

There are no special methods for the prevention of actinomycosis of the skin. To prevent the development of the disease, it is necessary to observe the rules of personal hygiene.

It is also important to maintain a good level of immunity. To do this, it is necessary to treat infectious and somatic diseases in a timely and correct manner.

It is especially important to monitor the good condition of the oral cavity and pharynx. Actinomycetes live and multiply on mucous membranes. The absence of diseases in the oral cavity will prevent the growth of the fungus and its further spread throughout the body.

Timely treatment and prevention of actinomycosis will help to avoid severe consequences of the disease.