Actinomycosis of various localizations. Actinomycosis - symptoms, routes of transmission and treatment Actinomycosis treatment drugs

Actinomycosis is an infection that penetrates tissues and organs, forming granulomas, abscesses, fistulas and causing the release of pus. The causative agents of the disease are anaerobic bacteria Actinomyces (actinonomycetes). A small amount of them (normally) is contained in the oropharynx and intestinal tract each person. Actinomycosis is a chronic disease that is difficult to treat in its later stages and often causes complications and relapses.

Causes

The habitat of actinomycetes, in addition to the human body, is soil and plants. Therefore, in addition to self-infection, actinomycetes can enter the human body through breathing, through food, and through wounds on the skin. Animals can also suffer from actinomycosis, but there have been no documented cases of actinomycosis being transmitted from animals to humans.

In most cases, actinomycetes that enter the body do not cause the development of the disease, but during the inflammatory process in oral cavity, gastrointestinal tract or in the respiratory organs, actinomycetes can multiply greatly and provoke the development of actinomycosis.

Actinomycetes are sensitive to high temperature (at 70-80ºC they die in 5 minutes) and a three percent formaldehyde solution. Actinomycetes are resistant to drying, and low temperatures preserve them for 1-2 years.

Most cases of actinomycosis are recorded in men (urban residents): men get sick twice as often as women. Actinomycosis in children and adolescents most often develops in the form of nodular infiltrates of brown or lilac color on the skin.

Localization of actinomycosis and its symptoms

Incubation period actinomycosis is not known. The disease begins with few symptoms and can progress over 10-20 years. In the absence of treatment for actinomycosis that has spread to internal organs, death occurs.

The most common localization of actinomycosis (in 55% of cases) is the cervical-facial localization, followed by abdominal localization in second place (20% of cases) and thoracic localization in third place (15%). In addition, actinomycosis can develop on the skin, in the genitourinary system, in the central nervous system, in bones and joints.

With cervicofacial localization of actinomycosis, the pathological process can occur with damage to the skin, subcutaneous and intermuscular tissue. In this case, in addition to the skin of the face and neck, the tongue, lips, eye sockets, larynx and trachea are affected. Cervicofacial actinomycosis can lead to facial asymmetry.

With abdominal localization of actinomycosis, symptoms may resemble an acute attack of appendicitis or intestinal obstruction. Abdominal actinomycosis can involve the liver, kidneys, intestines and spine.

Symptoms of actinomycosis with its localization: weakness and cough. At first the cough is dry, then it becomes moist with the release of mucopurulent sputum with a coppery taste.

Actinomycosis of the genitourinary system – quite rare disease, which develops when the disease spreads from abdominal cavity sick. With actinomycosis of the genitourinary system, pain occurs in the lower abdomen, the process of urination is disrupted, and bluish-colored tumor-like formations form. An abscess may rupture into the bladder or rectum.

When infection spreads from other organs, actinomycosis of joints and bones develops. Symptoms of actinomycosis of bones are similar to the symptoms of osteomyelitis; the bones of the skull, ribs, and upper extremities can be affected. Actinomycosis of joints is asymptomatic and does not cause significant loss of their functions.

Actinomycosis of the central nervous system is characterized by increased body temperature, headache, dizziness, convulsions, loss of consciousness, and loss of coordination. With actinomycosis, the central nervous system is affected by the brain or spinal cord: a cavity filled with pus is formed.

Diagnostics

Diagnosis of actinomycosis is carried out by external signs: on early stage actinomycosis has the appearance of a dense, painless edema, which over time becomes bluish in color, and at a late stage a fistula is formed. Before treating actinomycosis, it is necessary to ensure that the diagnosis is correct (actinomycosis should be differentiated from other mycoses).

Laboratory confirmation of actinomycosis in 25% of cases can be done by analyzing the discharge of fistulas (if actinomycosis affects internal organs, then the material is collected using a puncture biopsy of the affected organ): drusen of actinomycetes are detected in it. In most cases (75%), drusen of actinomycetes are not detected; in this case, purulent discharge or biopsy material is cultured.

Treatment

Traditional treatment for actinomycosis consists of daily intravenous administration penicillin for 2-6 weeks. After the end of the injections, oral antibiotics (penicillin, amoxicillin) continue for another 6-12 months. The patient is also prescribed several courses of intramuscular or subcutaneous administration of actinolysate (a drug made from the cult of anaerobic actinomycetes). Physiotherapeutic methods such as iodine electrophoresis and ultraviolet irradiation of the skin are effective in the treatment of actinomycosis. Doses medicines are selected individually. A special diet for actinomycosis has not been developed.

For advanced actinomycosis, surgical treatment is performed: opening of abscesses and drainage of fistulas. For actinomycosis armpit or groin area, the lesion is excised and cleaned, after which a suture is applied. Depending on the location of actinomycosis, patients may require several operations. After surgical treatment In serious cases of actinomycosis, radiotherapy is recommended.

Prevention

Specific prevention of actinomycosis has not been developed. General recommendations include timely treatment of infections of the oral cavity, gastrointestinal tract and respiratory system. It is necessary to maintain personal hygiene and, if possible, avoid injury to the skin, as well as increase immunity.

ACTINOMYCOSIS, ACTINOBACILOSIS AND RELATED DISEASES

Part /1 / 2 / 3 /

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

APPENDIX TO SECTION:

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

General overview

Actinomycosis, actinobacillosis, actinomycetoma and nocardiosis are diseases that are not related to each other in terms of etiology, epidemiology and therapy, but there are serious reasons for considering them together, since they have general history and nomenclatural 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, German veterinarian Otto Bollinger discovered that chronic tumor-like lesions on the jaws of cattle, thought of as a kind of sarcoma, contained 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. Botanist Carl O Harz (1877) believed that this was a new type of mold and proposed a generic and species designation Actinomyces bovis(radiant mushrooms, from Greek aktis = ray; mykes = mushroom) due to the striking radial divergence of the filaments in the granules. He also introduced the term "actinomycosis" for the disease for the first time.

First detailed description similar 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 animal pathogen A. bovis are anaerobes, or at least facultatively anaerobic capnophiles, bacteria that grow better in high CO2 conditions (Bujwid 1889, Mosselman and Lienaux 1890). It was only several decades later that it was established that the causative agents of human and bovine actinomycosis were separate species and that they were true, although filamentous, bacteria rather than 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 are still often referred to simply as "actinomycetes".

Lignieres and Spitz in 1902 described a new disease of cattle in Argentina, clinically and pathologically resembling bovine actinomycosis. The organisms cultured from the corresponding lesions were tiny, short, gram-negative bacterial rods that were noticeably different from A. bovis. Because of the similarity between the clinical pictures of these two diseases, the pathogen was first named "actinobacillus" and then officially designated as Actinobacillus lignieresii(Brumpt 1910).

Before the anaerobic nature of the causative agents of actinomycosis in humans and animals 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 were exogenous sources of actinomycotic infection and that chewing grass or grain could cause actinomycotic damage. This version was maintained long time even after the studies of Naeslund (1925, 1931) who proved that A. israelii is part of the innate microflora of the human oral cavity, which is not found in environment, and thus the source of actinomycosis is always endogenous.

By the end of the 19th century, several researchers had identified pathogenic aerobic actinomycetes similar to the causative agents of actinomycosis isolated by Bostroem. Nocard (1888) described an aerobic filamentous microorganism in "farcin du boeuf", a disease of cattle on the island of Guadeloupe. This pathogen is named Nocardia farcinica Trevisan (1889). A similar branching bacterium was isolated from a diseased human lung by Eppinger (1891), and this pathogen was subsequently designated Nocardia asteroides Blanchard (1896). Another filamentous, branching bacterium, first designated as " Streptothrix madurae", was isolated by Vincent (1894) from tumor-like lesions in India called "Madura 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 species 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 pathogens in both humans and animals. This does not only apply to some members of traditional clans 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 increasing range of pathogenic actinomycetes, it would hardly be advisable 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 be inaccurate to use the term “actinomycosis” for any type of infection caused by actinomycetes, as was common practice in the past. Likewise, the term "nocardiosis" does not cover all types of nocardial infections, nor infections caused by other anaerobic actinomycetes. Thus, the classical designations of the disease “actinomycosis” and “nocardiosis” should be retained to designate a specific, clinically and etiologically, disease with a characteristic clinical picture.

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 which usually causes suppuration and abscess formation and also 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 be caused by a diverse number of species of other fermentative 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” rather defines a polyetiological inflammatory syndrome than just a disease related to a separate pathogenic microorganism. To avoid introducing additional etiological terms and remain bacteriologically correct, it has been proposed to designate a group of closely related inflammatory processes by the term “actinomycosis” in plural(Schaal and Beaman 1984, Schaal 1996).

Actinomycosis in humans

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

Clinical manifestations of actinomycosis

Initial actinomycotic lesions usually develop in tissues adjacent to the mucous membranes, which are the natural habitats of the causative agents. The most commonly affected areas are the cervicofacial, thoracic and abdominal. Rarely - skin, bones, or central nervous system(CNS), which may also be involved in the pathological process (Slack and Gerencser 1975, Pulverer and Schaal 1984, Schaal and Beaman 1984, Schaal and Pulverer 1984, Schaal 1996). After the pathogen penetrates the tissue, the infection tends to progress slowly, regardless of the natural boundaries of the organ. Hematogenous spread is sometimes observed, in which the central nervous system (brain abscess) or natural cavities (empyema) may be involved. There is a characteristic tendency to both remission and exacerbation of symptoms, regardless of the treatment antibacterial therapy. Due to the fact that actinomycosis in humans is an endogenous infection, it is difficult or impossible to determine their incubation period. It is believed that before the appearance of the first clinical signs It lasts approximately 4 weeks, but numerous reports suggest that this period may be much longer or much shorter.

Cervicofacial actinomycosis

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

Table 1 Localization of actinomycosis in humans

Localization	Number of cases	%
Cervicofacial	3249	97,6
Thoracic, including chest wall	43	1,3
Abdominal, including pelvic organs	22	0,7
Limbs, skin	22	0,7
Brain	4	0,1
Blood (septicemia)	2	0,06
Total	3329	100,0

Data collected at the Institute of Hygiene, University of Cologne, 1969-84, and at the Institute of 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, damage to the mucous membrane by foreign bodies (bone fragments, fish bones, grass or grain awns) or suppuration of the tonsils. It should be remembered that traumatic factors, local or general predisposing conditions, do not necessarily occur in all cases or may be missed when collecting anamnesis.

In cervicofacial actinomycosis, according to an 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 areas that are less commonly affected: neck, mastoid, sinuses, parotid gland, thyroid gland, tongue, lips, nasal septum and ears (Slack and Gerencser 1975, Kingdom and Tami 1994). Direct damage to bone and regional lymph nodes is very rare, but periostitis and post-traumatic osteomyelitis with the presence of fermenting actinomycetes are not so rare (11.7% of cases reported by Herzog 1981).

Primary cervicofacial actinomycotic lesions are either acute, predominantly odontogenic, abscesses, or very sharp forms panniculitis, or as a slowly developing hard, reddish or livid inflammatory infiltrate (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 the masticatory muscles when the process forms near the temporomandibular joint.

To achieve rapid and complete healing, surgical incision and drainage alone are not sufficient in the vast majority of cases. Acute and especially chronic cases tend not to heal without specific antibiotic therapy. At best, there is a temporary regression of symptoms, 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 hard, painless, livid infiltrates on the periphery, the formation of multiple areas of softening and the formation of fistulas. The latter appear spontaneously or form at the site of a 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 introduction of “standard” antibiotics, and shows a clear tendency to relapse after temporary regression of inflammatory signs . Without treatment or with inappropriate treatment, cervicofacial actinomycosis progresses slowly, even across organ boundaries, and can become life-threatening when introduced into the cranial cavity, mediastinum or when invading large blood vessels (Herzog et al., 1984). Discharge from fistulas and pus from abscesses are usually yellowish in color and the consistency of serous discharge is thicker and often contain particles originally called “drusen”, or often referred to as “sulfur granules”.

Thoracic actinomycosis

Thoracic lesions with 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, dental plaque or calculus, the contents of the tonsil crypt or foreign body, contaminated with oral microflora, including pathogenic actinomycetes. Sometimes, this form of the disease develops due to local spread of a cervicofacial process, perforation of the diaphragm due to injury to the abdominal cavity, or hematogenous spread from any distant site of infection (Slack and Gerencser 1975).

Primarily, 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 isolated dense or multiple shadows in which cavities may form. At the onset of the disease, the main signs are chest pain, fever, cough with or without sputum, and weight loss, but hemoptysis is unusual. The infection may subsequently progress to pleural empyema, pericarditis, or chest wall lesions. 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 drain pus containing large numbers 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 injuries from swallowed bone fragments or fish bones.

Another source of pelvic and abdominal actinomycotic infections has recently been identified. It has been found 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 et al. 1989, 1992, Schaal and Lee 1992, Chatwani and Amin-Hanjani 1994), as well as other, predominantly anaerobic, bacteria (Schaal and Lee 1992). They practically never occur in women who do not use these devices. This colonization may serve as the initial site for the development of aggressive actinomycosis affecting the pelvic organs 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 mild and vague. They include: fever, malaise, weakness and pain, which slowly but progressively increases. As the process progresses, it usually resembles slowly progressing tumors similar to malignant processes, such as cancer of the stomach, colon, rectum, anorectum 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, large livid masses, or fistulas may be observed, from which drusen discharge is often the first characteristic sign of the disease (Schaal and Beaman 1984). Without effective treatment Abdominal actinomycosis can spread to any adjacent tissue or organ, including the liver, spleen, kidney, fallopian tubes, ovaries, uterus, testes, bladder, rectum, or abdominal wall (Slack and Gerencser 1975, Khalaff, Srigley and Klotz 1995, Müller -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 accessible effective antibacterial 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 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 the location, and are determined by the speed of development of the abscess, the degree of displacement or destruction of brain tissue. Main symptoms - headache, increase intracranial pressure, focal symptoms, hemiparesis, aphasia, ataxia and pathological 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 caused by 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 may be observed, surrounded by denser bone tissue. 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 injuries sustained in a fist fight. Hematogenous spread of the pathogen into the skin may also occur. The clinical picture of cutaneous or wound actinomycosis is very similar to the cervicofacial form.

Epidemiology of actinomycosis

Bacteria that are isolated from foci of actinomycotic lesions in humans essentially belong to the resident or transient innate microflora of the mucous membranes. Thus, except for actinomycosis resulting from human bites or injuries in a fist fight, the disease is always of endogenous origin and therefore is not capable of epidemic outbreaks or transmission in the usual sense.

Although sporadic actinomycosis occurs throughout the world, the incidence of actinomycosis appears to vary from continent to continent, country to country, or even region to region, perhaps 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 United States compared with Europe, but the higher prevalence of thoracic and abdominal infections on the North American continent.

Based histological studies Hemmes (1963) calculated the incidence of actinomycotic infections in the Netherlands as 1 per 119,000 inhabitants per year. For the Cologne region in Germany before 1969, Lentze (1969) reported an incidence of 1 in 83,000. This incidence was subsequently 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 determined (Schaal 1979). This is significantly higher than the incidence of actinomycosis in other areas of Germany and other European countries. Such differences are difficult to explain but may be due to local diagnostic differences 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 often in men than in women. In addition, epidemiological data show that the unequal distribution of the disease by gender is limited only to patients of puberty. Before puberty and at 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 women aged 11 to 30 years (Pulverer and Schaal 1978, Schaal 1981, 1992, Schaal and Beaman 1984).

Pathology and pathogenesis

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

Drusen of actinomycetes can be found in a purulent focus. They are found in the contents of an abscess or in discharge from fistulas in approximately 25% of cases, which has great diagnostic value. Drusen measure up to 1 mm in diameter and are visible to the naked eye. These are yellowish (with a reddish or brownish tint) particles that resemble cauliflower at low magnifications. Under the microscope, after slight compression between the slide and cover glass, one can see that they are composed of a varying 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 granules at high magnification show that the material consists of groups 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 leukocytes. 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 by 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,” quite widely used to designate actinomycotic drusen, refers only to the yellow color of the particles, and not at all to the high sulfur content in them.

The main natural habitat of all fermenting actinomycetes pathogenic to humans is the oral cavity of healthy adults, where they live in significant quantities. In the digestive and reproductive tracts, however, they appear to be present only sporadically or in low quantities. The same applies to the oral cavity of pre-teething infants and edentulous adults. This may explain why cervicofacial actinomycosis is relatively less common in very young or old people.

The relatively low incidence of the disease compared to the widespread occurrence of the pathogen in adults is apparently due to 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 penetration than on a defect in the function of the immune system as a whole. In this regard, a mandatory 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. This local decrease in oxygen potential may be caused by impaired circulation due to general circulatory disorders or vascular disease, traumatic injuries with tissue crushing or the introduction of foreign bodies, or the necrotic ability of other simultaneously present microorganisms.

These so-called “associated microorganisms” are, as it were, a trigger for 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 that determines the characteristics clinical course and 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. Most often 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 encountered quite rarely. Previously classified as Arachnia propionica(Schaal 1986), it was recently transferred to the family 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 whether they are simply members of a mixed bacterial flora of no particular importance.

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

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

Kinds	Actinomycotic lesions (n=1376)%	Conditions associated with intrauterine contraceptives (n=114)%	Eyes, lacrimal organs (n=98)%
Actinomyces israelii	73.3	54.4	13.3
A. gerencseriae*	2.0	7.0	11.2
A. naeslundii	6.8	6.1	16.3
A. viscosus	4.9	16.7	19.4
A. odontolyticus	1.4	2.6	12.2
A. meyeri	0.6	3.5	0.0
A. georgiae	0.2	0.0	0.0
A. neuii	0.2	0.0	0.0
Propionibacterium propionicum	3.3	4.4	16.3
Bifidobacterium dentium	0.4	2.6	2.2
Corynebacterium matruchotii	0.9	0.0	2.2
Rothia dentocariosa	0.4	0.6	5.1
Not identified	5.7	2.0	2.0
Total	100.0	100.0	100.0

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

*Note: differences between A. israelii And A. gerencseriae not generally produced before 1987.

The accompanying microflora in the foci of actinomycosis can 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 types of associated bacteria were present in the outbreak, but in some cases up to 10 were identified.

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

Kinds
No aerobic growth	47,2	32,1
Coagulase-negative staphylococci	27,9	14,8
Staphylococcus aureus	12,7	6,2
alpha-hemolytic streptococcus	11,2	11,1
beta-hemolytic streptococcus	4,9	11,1
Streptococcus pneumoniae	0,0	0,0
Enterococci	0,0	16,1
Skin corynobacteria	0,0	3,7
Haemophilus spp.	0,1	1,2
Enterobacteriaceae	2,5	13,6
Gardnerella vaginalis	0,0	6,2
Non-fermentative	0,2	0,0
Yeast	0,1	0,0
Total	100,0	100,0

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 are much more diverse and numerous. Synergistic interactions likely exist between A. israelii And A. gerencseriae With Actinobacillus (Haemophilus) actinomycetemcomitans. The latter microorganism, whose name refers to its characteristic resemblance to actinomycetes, is often the cause of especially chronic course disease and ineffective treatment. This pathogen can maintain an inflammatory process with similar symptoms even after chemotherapy completely eliminates the actinomycetes. Other common companions of actinomycetes are black pigmented Bacteroidaceae (Prevotella spp., Porphyromonas spp.), non-pigmented 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

Kinds	Cervicofacial actinomycosis (n=3197) %	Conditions associated with intrauterine contraceptives (n=81) %
Actinobacillus actinomycetemcomitans	22,9	2,5
Microaerophilic streptococci	29,3	22,2
Peptostreptococcus spp.	18,2	29,6
Black pigmented Bacteroidaceae	37,7	58,0
Unpigmented Bacteroides/Prevotella spp.	14,0	69,1
Fusobacterium spp.	32,5	22,2
Leptotrichia buccalis	20,4	2,5
Eikenella corrodens	16,5	46,9
Capnocytophaga spp.	0,4	6,2
Campylobacter/Selenomonas spp.	0,1	3,7
Propionibacterium spp.	30,5	24,7
Bifidobacterium spp.	0,1	1,2
Lactobacillus spp.	0,5	42,0
TOTAL	100,0	100,0

According to Schaal and Lee (1992).

Very little is known regarding the humoral and cellular immune responses of patients suffering from actinomycosis. Antibodies against fermenting actinomycetes can be detected in human serum various methods, including immunofluorescence methods and linked immunosorbent assay. 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 primarily 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 a sign of self-cure of this disease.

On the other hand, it was established quite a long time ago (Lentze 1938) that the immune system of patients with actinomycosis can be stimulated by the introduction of formalin-killed cells or cell extracts 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 that forms after repeated administrations helps overcome the disease. These observations provide the basis for 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 often misleading and histopathology and serology low in specificity and sensitivity. The presence of drusen, which sometimes gives pus appearance semolina porridge should initiate a search for actinomycetes. However, given that only 25% of actinomycotic pus samples contain these granules, their absence does not exclude the diagnosis of actinomycosis.

Collection and transportation of pathogenic material.

Pathological material suitable for bacteriological analysis of actinomycosis is pus, discharge from fistulas, bronchial secretions, granulation and biopsy samples. During collection, precautions should be taken against contamination by innate mucosal microflora. Whenever possible, pus or tissue should be obtained by percutaneous puncture. To diagnose thoracic actinomycosis, bronchial secretions must be obtained transtracheally. Examination of sputum is unreliable because it usually contains oral actinomycetes, including pathogenic species. Transthoracic percutaneous needle biopsy or percutaneous puncture of suspicious abdominal abscesses are often the only means of obtaining satisfactory specimens for diagnosis. Transport of samples to the bacteriological laboratory must be fairly rapid. If long-term transport is unavoidable, special transport media such as Stewart's should be used, although fermenting 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 cover glass and with a 1% solution of methylene blue added to a drop. Actinomycotic drusen appear as cauliflower-like particles with an uncolored 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 granules 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 associated 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 to detect specific antibodies can also be used to identify the actinomycete species present in the granule without isolating a culture.

Cultural diagnostics

To obtain reliable results, it is advisable to use clear media so that the plates can be carefully examined for the characteristic thread-like colonies, and to grow the culture for at least 14 days. Cultures can be examined every 2-3 days without changing 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 simultaneously and examine them for actinomycete growth after 3, 7 and 14 days. Since removing the plates from the anaerobic environment usually stops further growth of microorganisms that require long-term incubation without changing 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 actinomycete species may take 14 days or more. This is necessary to reliably identify 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. Detailed bacteriological analysis of the accompanying microflora may also be useful for selecting appropriate antibiotic therapy.

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

Serological diagnosis.

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

Treatment

Surgical dissection of actinomycotic lesions and drainage of purulent contents is always the basis of treatment for actinomycosis. However, it is known that even radical surgery often only results in a temporary reduction of 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, and arsenic preparations, which, however, did not improve long-term results. Only subcutaneous administration of killed actinomycete cells (heterovaccine Lentze 1938) showed some effectiveness.

Progress in the treatment of actinomycosis occurred when sulfonamides and penicillin became available. Penicillin was active against pathogenic actinomycetes in vitro And in vivo. Given that many patients had little or no response to penicillin therapy, treatment with high doses of penicillin for at least 3 months and up to 12–18 months was often recommended (Harvey, Cantrell and Fisher 1957).

Poor response to penicillin treatment is often due to the presence of associated bacteria that are penicillin-resistant. In addition, drugs do not penetrate well through the dense tissue of actinomycotic lesions and into drusen. Finally, A. actinomycetemcomitans- usually resistant to penicillin, although they do not produce beta-lactamases. Thus, penicillin in the treatment of actinomycosis is effective only when there is no 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 the growth A. actinomycetemcomitans. However, given that they are not resistant to beta-lactamases, microorganisms that produce beta-lactamases may interfere with their therapeutic effectiveness. This is rarely the case in cervicofacial actinomycosis, but in thoracic and especially abdominal infections, beta-lactamase producers are usually present. Therefore, currently used treatment regimens include drugs effective against actinomycetes and potential producers of beta-lactamase type S. aureus, gram-negative anaerobes, and, in cases of abdominal actinomycosis, Enterobacteriaceae.

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 starting dose is 2 g amoxicillin three times daily plus 0.2 g clavulanic acid three times daily for 1 week, and 1 g amoxicillin three times daily plus 0.1 g clavulanic acid three times daily for another week. In rare cases chronic infections The cervicofacial area 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 period - 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 necessary, especially when there is persistent presence Enterobacteriaceae type Klebsiella spp. or Enterobacter spp. The latter are generally usually present in abdominal actinomycosis. The therapy of choice for treating these infections is a combination of amoxicillin and clavulanic acid with metronidazole (or clindamycin) for strict anaerobes, plus tobramycin or gentamicin. Imipenem may be a suitable alternative, but it is still rarely used for the treatment of 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 infections 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). To treat patients allergic to penicillins, tetracyclines or cephalosporins can be used instead of aminopenicillins, but the clinical effectiveness of these drugs is much less than that of aminopenicillins or the combination of aminopenicillins with beta-lactamase inhibitors.

Forecast

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

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 be classified under the term "actinomycosis". However, some of them are no less important than actinomycosis, both from medical and economic points of view.

Canaliculitis and other eye infections

Most frequent illness, 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 adhesions 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 areas of the lesion is very similar.

In addition to lacrimal canaliculitis, ocular infections caused by fermenting actinomycetes may also present as conjunctivitis, keratitis, dacryocystitis, inflammation of the mucous glands of the eyelid, and even periobital abscess, granuloma, or intraocular infection (Schaal 1986, Schaal and Lee 1992). Reliable diagnosis lacrimal canaliculitis and other actinomycotic eye lesions are carried out in accordance with the bacteriological procedures mentioned above. Removal of lacrimal adhesions, which are usually present in canaliculitis, and local application of antibiotics almost always results in a rapid 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 previously in the section on abdominal actinomycosis, the uterus and cervical canal of women with intrauterine contraceptives or vaginal uterine rings are often colonized by a complex bacterial flora, which consists of fermentative actinomycetes and various other aerobic and anaerobic bacteria (Eibach et al. 1989, Schaal and Lee 1992). These microorganisms are especially abundant directly on the IUD thread within the cervical canal, and are very reminiscent of 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 (see Table 2). The accompanying 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 usually present (Table 4), it should be noted that the frequency of isolation is much lower A. actinomycetemcomitans and even lower frequency of detection of fusobacteria in ICH than in cervicofacial actinomycosis, while non-pigmented species Bacteroides And Prevotella, E. corrodens and lactobacilli are more often isolated from ICH. The presence of fermenting actinomycetes and characteristic associated bacteria on the IUD 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 cervical canal 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 disappear within 4-8 weeks after removal of the IUD, at least for infections of the lower genital tract.

When typical actinomycetes are found on the IUD or in the cervical canal, the use of the IUD should be discontinued. After the microflora returns 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, urethritis, funisitis (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 grevenitzii(Ramos et al. 1997). It has also been described as a new actinomycete-like species 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 represented in nature, especially in 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 the families Cellulomonadaceae, Dermatophilaceae, Nocardiaceae, Gordoniaceae, Tsukamurellaceae, Pseudonocardiaceae, Streptomycetaceae, Nocardiopsaceae And Thermomonosporaceae. Depending on the actinomycete species involved, its site and mechanism of entry, and the immune status of the host, aerobic actinomycetes can cause a variety of diseases in humans and animals. In addition, it has recently been recognized that these microorganisms may be a cause of hospital-acquired infections, such as catheter-associated sepsis or post-operative wound infections. The most common pathogens responsible for these diseases belong to the genera Nocardia And Actinomadura, but other actinomycetes such as Amycolatopsis, Gordonia, Nocardiopsis, Pseudonocardia, Rhodococcus, Saccharothrix, Streptomyces And Tsukamurella(Schaal and Lee 1992, McNeil and Brown 1994).

Actinomycosis

Actinomycosis is a chronic disease of cattle, pigs and animals of other species, as well as humans, characterized by the formation of specific granulomas in various tissues and organs (skin, bones, parenchymal organs).

Actinomycetes (Greek mykos - mushroom; actis - ray) are single-celled microorganisms - radiant fungi.

Order Actinomycetales

Family Actinomycetaceae

Genus Actinomyces

The disease is most often caused by Actinomyces bovis. It is a coccus-like or branching filamentous form.

In the affected tissues it has the appearance of rods and threads or forms characteristic clusters in the form of a bush or rosette (drusen), consists of a central ball of Gr+ threads. Drusen can be seen with the naked eye in the pus, where they are present in the form of small grains of yellow-ashy or Brown. Thread width 0.2-1.2; length 100-600 microns.

Cultivation

Isolation of the primary culture of actinomycosis is carried out under anaerobic conditions at a temperature of 37°C, inoculated on Sabouraud agar or glucose-blood agar. Culture develops slowly. On the 15-20th day after sowing, small yellowish colonies appear in the thickness of the agar. The colonies firmly grow together with the environment, their surface is as if sprinkled with lime powder - this is aerial mycelium, at the ends of which spores develop, giving the colonies a yellowish or red color.

Can be grown on Kitta-Tarozzi medium, MPA (with the addition of whey), MPZh, MPB, in milk and on potatoes.

Biochemical activity is weakly expressed. Ferments with the formation of CG - glucose, galactose, glycine, liquefies the uterine fluid.

Antigenic structure

The pathogen has two serological variants: 1 and 2, which differ in surface antigens. They can be identified in the RIF.

Sustainability

Actinomycetes are resistant to desiccation, especially their spores. At a temperature of 70-80°C, actinomycetes die after 5 minutes, Sun rays kill them after 3 hours, 5% chloramine solution - after 3 hours, 5% Lysol solution - after 30 minutes, 3% formaldehyde solution - after 20 minutes.

Pathogenicity and pathogenesis

Pathogenicity has not been sufficiently studied. It is believed that pathogenic actinomycetes contain endotoxin, a necrotoxin-type exotoxin, which promotes tissue necrosis.

Spreading. The causative agent of actinomycosis is widespread in nature. It is found in soil, water, rotting fruits, cereal grains, in animal organisms in the oral cavity, dental cavities, tonsils, in the upper respiratory tract, and urinary tract.

Infection occurs through penetration of the pathogen when the integrity of the skin is broken, through the mucous membrane of the oral cavity, pharynx or intestines. The pathogen spreads throughout the body through the bloodstream, forming metastases in internal organs, bone tissue or skin.

Actinomycosis affects large cattle, but can infect pigs, horses, goats, dogs, and rabbits.

Pathogenesis. Once in damaged tissue, actinomycetes settle at the site of penetration or migrate through the intercellular spaces into various tissues. For damaged lymphatic vessels The pathogen reaches the lymph nodes, and once it enters the bloodstream, it reaches various parts of the body. At the site where actinomycetes invade, colonies in the form of drusen are formed. Along the periphery of the drusen, the mycelium forms a dense plexus, and in the center it is more sparse.

In an actinomycosis lesion, proliferative phenomena develop, accompanied by the formation of granulation tissue. In the center of the infiltrate, purulent softening of the tissue occurs, which leads to the breakthrough of pus to the outside.

Laboratory diagnostics

The diagnosis is made based on clinical signs and the presence of drusen in areas of swelling. For this purpose, microscopy of stained and unstained preparations from pus and histological sections of pieces of affected tissue are performed.

Isolation of a pure culture and bioassay are rarely carried out.

The duration of a complete laboratory study is 15-20 days, microscopic - 1 day.

Immunity and remedies specific prevention

After past illness does not form, the disease may recur. In animals that have recovered from the disease, precipitins, agglutinins, and KS antibodies are formed in the blood, which are not indicators of resistance. During the course of the disease, delayed-type hypersensitivity develops.

There are no specific means of prevention and therapy. To date, the main treatment method has been surgery.

For treatment, antibiotics can be used in combination with sulfonamide drugs.

Iodine therapy gives good results, especially in the initial stage before the formation of actinomycosis abscess.

Actinomycosis is an infectious disease caused by actinomycetes (radiant fungi). It occurs in acute and chronic forms, manifests itself as dense granulomas, fistulas and abscesses, affecting the skin and internal organs. For diagnosis, inoculation on nutrient media is used; it allows one to detect characteristic mycelium in the discharge and the growth of specific colonies. For treatment, immunostimulants and antibiotics are used, skin irradiation with ultraviolet light and electrophoresis are prescribed. In severe cases it is required surgical intervention– treatment of fistulas, opening of abscesses, drainage of affected cavities.

Features of actinomycosis

The causative agents of actinomycosis are the radiant fungi Actinomyces albus, Actinomyces bovis, Actinomyces israelu, Actinomyces violaceus. In the presence of a nutrient medium, they actively multiply and form colonies of various shapes with protrusions similar to rays. This type of pathogenic microorganisms is found not only in humans, but also in animals. Most often - in the form of yellowish lumps (drusen) with a diameter of 1-2 mm. When examined through a microscope, clusters of mycelial filaments are visible in the center of the lumps, and flask-shaped swellings are visible at the edges. There are drusen without radiate projections. Radiant mushrooms die when exposed to benzylpenicillin, chloramphenicol, streptomycin, tetracycline, erythromycin. The incubation period can last from several days to several years. Therefore, for a long time, the state of health with actinomycosis does not worsen, and the disease does not manifest itself in any way.

There are more than ten clinical forms of actinomycosis:

• Cervicofacial (maxillofacial).
• Skin.
• Osteoarticular.
• Thoracic.
• Abdominal.
• Genitourinary.
• Nervous (actinomycosis of the central nervous system).
• Mycetoma (Madura foot or actinomycosis of the foot).
• Other, rarer forms.

Actinomycosis is widespread and affects people and farm animals. The causative agent of the disease is present in the environment, in the human microflora - in the mouth, on the tonsils, and in the gastrointestinal mucosa. There are internal and external methods of infection. What they look like various shapes actinomycosis, can be seen in the photos below.

Symptoms of actinomycosis

From the moment radiant mushrooms enter the body until the first symptoms appear, several weeks or even years can pass. On initial stage purple or bluish spherical infiltrates are formed (seals resembling atheromas). They cause aesthetic discomfort, but do not worsen well-being. After some time, the seals soften and then open. Fistulas form inside the infiltrates, and bloody pus is released from them. Sometimes grains are found inside the fistulas yellow color– these are accumulations of pathogenic fungi. Over time, necrosis develops, and ulcers form at the site of the fistula. TO characteristic symptoms Cough can also be attributed. At first it is dry, then becomes wet with the release of sputum, the smell of which is similar to the smell of earth. When going to chronic form seals and fistulas appear on the chest, lower back and hips. If symptoms of actinomycosis appear, you should immediately consult a doctor and receive qualified treatment.

Causes of actinomycosis

The name of the pathogens suggests that they form colonies in the form of a cluster of threads with flask-shaped processes. When stained with hematoxylin-eosin, the clusters appear blue and the rays appear pink. Thanks to this, under a microscope, colonies take on a very unusual appearance. Pathogenic fungi (actinomycetes) are present in the normal human microflora, but in a calm state they do not pose a danger. They can be found in the oral cavity, on dental plaque during caries, on the tonsils, bronchi, stomach, rectum and anus. In nature, ray-shaped mushrooms are present in soil, water, and dry grass. Therefore, infection can be both exogenous (multiplication of fungi on the surface of the skin) and endogenous - the development of the disease from within the body. The most effective remedy fight against radiant mushrooms - antibacterial drugs. In many cases, the source of infection cannot be identified. Sometimes this is contact with a carrier of actinomycosis, sometimes it is an infection from the environment.

There are a number of main routes of infection by actinomycosis:

• Contact (household).
• Airborne.
• Aerogenic (by inhaling contaminated dust).
• Entering the body with food and water.

In the absence of favorable conditions for actinomycetes, they remain dormant for some time (saprophytic existence). Under pathogenic influence, they actively multiply, cause local inflammation, and hematogenous or lymphogenous spread of infection occurs throughout the body.

Actinomycosis is diagnosed in men twice as often as in women; the risk group includes men and women aged 21 to 40 years. The effectiveness and results of treatment depend on immune system, the incidence of diseases increases in the cold season.

Actinomycosis in children

According to statistics, actinomycosis in children affects the lungs in 15% of cases, the intestines in 20%, and the face and neck in 50%. The affected area becomes bluish and hard to the touch. In the affected areas, fistulas with light yellow pus appear. In most cases, this is maxillofacial or bone actinomycosis. It is divided into cutaneous, subcutaneous and musculocutaneous, primary and secondary. The provoking factor in the primary case is diseased teeth, in the secondary case it is damage to soft tissues. A typical clinical picture of actinomycosis in children is actinomycotic granuloma.

As for bone tissue, in children it is resistant to the necrotic process. However, during the active course of the disease, large amounts of pus accumulate, which leads to the resorption of bones, the formation of cavities and fistulas in them. Bone actinomycosis has two forms. The first is characterized by pronounced plastic changes, the second is characterized by necrotic processes in bone tissue that are invisible at first glance (bone abscess). At the initial stage, the disease has no characteristic signs, so it is very difficult to identify it.

To reduce the risk of disease, you must first monitor the condition of your child’s teeth. With timely diagnosis and treatment, the skin and bones are restored. It takes a long time to heal a child. complex therapy with breaks for 1-2 months.

Diagnosis of actinomycosis

Only a doctor can diagnose the disease. Injuries, chronic infections, and surgical operations are important. At the initial stage, actinomycosis is difficult to detect, so the diagnosis can only be confirmed with characteristic lesion skin. For this purpose, laboratory and instrumental studies are prescribed:

• A culture of actinomycetes is isolated in the purulent contents of fistulas.
• Crops on Sabouraud's medium are being studied.
• A microscopic analysis of the grown colonies is carried out.

The preliminary result can be obtained in 3 days, the final result in 12 days.

In addition, it may be necessary to isolate a culture of actinomycetes. Macroscopically, granulomas, purulent transformations and tissue breakdown are detected. Microscopically, cell breakdown and necrosis, fibrosis and fibrous structures around the lesions are revealed.

There are 2 stages of actinomycosis – initial (destructive) and secondary (destructive-productive). In the first case, the formation of granulation tissue, a tendency to suppuration and cell disintegration is observed, in the second - the addition of plasmatic, lymphoid, xanthoma, epithelioid cells, collagen fibers, and drusen.

When making a diagnosis, the doctor may prescribe:

• RIF (immunofluorescence reaction to determine the species of actinomycetes).
• RSC with actinolysate (complement fixation reaction).
• X-ray (if damage to internal organs is suspected).
• Ultrasound (for the abdominal form of the disease).
• Clinical blood test, urine test, biochemical analysis blood (auxiliary methods).

Treatment of actinomycosis

Treatment of actinomycosis is a set of measures aimed at relieving symptoms and eliminating causes. The maximum effect is ensured by a combination of antibiotics and immune drugs. The treatment regimen depends on the form and extent of the disease.

• For the cervicofacial (maxillofacial) form - phenoxymethylpenicillin (2 g per day for 6 weeks), tetracycline (0.75 g 4 times a day for 4 weeks or 3 g per day for the first 10 days, then 0.5 g 4 times a day for another 3 weeks), erythromycin (0.3 g 4 times a day for 6 weeks).
• For the abdominal form and actinomycosis of the lungs - benzylpenicillin intravenously (10,000,000 units per day or more for 1-1.5 months), then - phenoxymethylpenicillin (2-5 g per day for 2-5 months).
• With the development of secondary staphylococcal infection- dicloxacillin or antibiotics of the tetracycline group, anaerobic - metronidazole.
• In case of disruption of the immune system, actinolysate is given subcutaneously or intramuscularly (3 ml 2 times a week for 3 months, at least 20 injections per course).
• For empyema and abscess - surgical intervention (opening, drainage).
• If lung tissue is damaged, lobectomy is performed.

The most effective drugs in the treatment of actinomycosis are tetracycline antibiotics, phenoxymethylpenicillin and erythromycin. There are currently no actinomycetes resistant to them.

Folk remedies

It is important to understand that traditional medicine is an auxiliary measure for drug therapy, but not a separate way to get rid of the disease. The basis of treatment is antibiotics, which increase the effectiveness and consolidate the result - traditional medicine recipes, but they can only be used after consultation with a doctor.

• Onion. Peel the onion, grind it into a paste, and squeeze it out. Lubricate damaged areas of the skin, use only freshly squeezed juice.
  Garlic. Pour 6 cloves of finely chopped garlic into 250 ml of alcohol or vodka, leave for 2-3 days in a cool, dark place, then store in the refrigerator, covered.
• Lubricate the affected areas or apply compresses, diluting with distilled water in a ratio of 1:2.
• Eleutherococcus. The finished tincture is sold at the pharmacy. Take 40 drops 2 times a day, this will increase immunity and speed up the healing process.
• Eucalyptus. Mix 2 tbsp. spoons of birch buds, horsetail and eucalyptus leaves, pour 500 ml of boiling water. If desired, add lemon balm and St. John's wort, let it brew, strain. Drink 60 ml each time after meals.

Complications of actinomycosis

Most mild form The disease is considered to be maxillofacial actinomycosis, but even its treatment does not exclude the development of relapses. If left untreated, health and life-threatening complications may occur. If the fungus affects internal organs, untimely treatment can lead to serious conditions and death. In general, the prognosis for recovery is favorable; to avoid complications, you need to be under the supervision of a doctor, follow his recommendations, and take preventive measures.

Prevention of actinomycosis

Prevention of actinomycosis does not require much effort; it is enough to lead a healthy lifestyle and refuse bad habits, monitor your health and perform simple rules. To prevent getting sick or speed up your recovery:

• Maintain good hygiene.
• Treat your teeth and gastrointestinal tract in a timely manner.
• Destroy all possible foci of infection as early as possible and carry out sanitation.
• Maintain your immunity, avoid hypothermia and too frequent colds.
• Get preventive medical examinations.

At bronchial asthma, chronic enterocolitis, liver cirrhosis, Crohn's disease and other related chronic diseases Visit your doctor regularly. Remember: if actinomycosis of the skin and other organs is not diagnosed in time, if you do not receive medical care At the initial stage, the disease can be fatal. Self-medication, as well as the use of drugs, will cause irreparable harm to health.

Actinomycosis (another name is radiant fungal disease) is a chronic pathology, the occurrence of which is provoked by different types of actinomycetes. With actinomycosis, damage to various organs and tissues consists of the formation of compacted infiltrates, which after some time suppurate with the appearance of fistulas (pathological tracts), as well as specific damage to the skin around them.

Table of contents:

Etiology. Characteristics of the pathogen

Most often, actinomycosis is caused by the following types of pathogen:

• Actinomyces Israeli;
• Actinomyces bovis;
• Actinomyces albus;
• Actinomyces violaceus.

This mushroom was called radiant because, growing on one or another nutrient medium, it forms peculiar colonies, often characterized by radiant edges. In the pathological material studied there are individual yellowish lumps with a diameter of 1-2 mm - they are also called drusen. At microscopic examination in the middle of the lumps, clusters of mycelial filaments (actually, the “body” of the fungus) are visible, which at the periphery of the drusen turn into swellings similar to flasks (sometimes they are absent). The microbiological picture when painted with a microbiological dye is unique and memorable: the center of the druse is blue, and the flask is pink.

Actinomycetes are characterized by sensitivity to such as:

• benzylpenicillin (better known as simply penicillin) - at a dose of 20 U/ml;
• streptomycin – at 20 µg/ml;
• tetracycline – at 20 µg/ml;
• chloramphenicol – at 10 mcg/ml;
• erythromycin – at 1.25 mcg/ml.

Actinomycetes cause disease not only in humans, but also in farm animals. However, cases of human infection from an animal, or from another person, have not been recorded. It is interesting that actinomycetes have been accidentally discovered more than once in other people when an examination was carried out to clarify another diagnosis. They were found:

• in the oral cavity;
• in plaque on teeth;
• on the palatine tonsils;
• on the mucous membrane of the digestive tract.

Epidemiology

The prevalence of the disease is widespread - actinomycosis is diagnosed in patients in all countries. Pathogens are widely distributed in nature. They were found in soil, on living plants, hay, straw and other natural structures.

Pathogenesis

With plants, actinomycetes enter the body and settle on mucous membranes in the form of saprophytes - a type of condition when a microorganism lives in the body of the “host”, but does not cause harm, living its life.

• inflamed;
• suppurates;
• multiple abscesses appear - limited small cavities filled with pus;
• the abscess wall cannot withstand the overflow of purulent contents and breaks through, fistulous tracts are formed.

A secondary infection occurs because the body is weakened by the fight against the infectious agent. In most cases this is . They contribute to the suppuration of infiltration granules created by actinomycetes. Pathological process it is further aggravated by the fact that the antigens of radiant fungi provoke a specific sensitization of the body, as a result of which it becomes more sensitive to any antigens - in particular, microorganisms that are attacking it at the moment. Allergic restructuring of the body manifests itself:

• delayed type hypersensitization;
• hypersensitization of the tuberculin type;
• the formation of antibodies (complement-fixing, agglutinins, precipitins and others).

Incubation period and clinical signs

The incubation period can vary widely - from 2-3 weeks to several years.

The following clinical types of actinomycosis are distinguished:

The disease belongs to primary chronic infections, therefore characterized by:

• long course;
• continuous progression.

A visual picture of the skin involvement gives a clear idea of ​​what tissue changes actinomycosis provokes:

Symptoms of maxillofacial actinomycosis

This is the most common form of actinomycosis. Based on the severity of the process, the following forms can be distinguished:

• cutaneous, or superficial;
• subcutaneous;
• muscular, or deep.

In the cutaneous form of actinomycosis, which is quite rare, the course is quite favorable in comparison with other forms . Infiltrates look like balls or have a hemispherical shape and are located shallow under the skin. Changes may include:

• cheeks;
• one or both lips;
• tongue throughout its entire length;
• tonsils;
• eye socket area;
• larynx.

With the muscular variety, pathological changes concern mainly the masticatory muscles (localized under the connective tissue fascia that covers them). They can form an infiltrate of increased density (the consistency is like that of cartilage) in the area of ​​the mandibular angle. The face takes on a characteristic appearance:

• it is asymmetrical;
• trismus is observed (muscle spasm that does not allow movement of the lower jaw).

Symptoms of actinomycosis of the central nervous system in the initial stages are as follows:

• increase in body temperature - first to low-grade levels, then higher;
• , which becomes more and more pronounced over time;
• seizures

At further development The disease exhibits pronounced signs of a central nervous system disorder:

• and not related to food intake;
• painful;
• frequent;
• lack of coordination (such patients may even fall).

Symptoms of actinomycosis of the genitourinary system

The urinary and urinary organs are rarely affected by actinomycosis, and damage to the genital organs is generally extremely rare.

Primary actinomycosis of the genital organs occurs as a secondary lesion in abdominal actinomycosis due to the active spread of infiltrate to them and means that the primary focus should be looked for in the abdominal cavity. Having been educated in the area Bladder, the infiltrate can spread to the tissue around the prostate in men and the uterus in women, but the prostate and uterus themselves may not be affected, despite the proximity of these organs to the pathological process.

Symptoms:

• aching;
• purulent discharge from the urinary tract;
• in the later stages - the formation of fistulas of the soft tissues of the abdomen in the pelvic area.

What is mycetoma (maduromatosis, Madura foot). Symptoms

Mycetoma is a peculiar type of actinomycosis that affects the foot. As a nosology, it has been known for a long time, and was especially often found in patients living in tropical latitudes.

The onset of the disease is manifested by the appearance of nodes on the foot (mainly on the sole) with characteristic signs:

• dense in consistency;
• having clear boundaries;
• pea-sized or larger;
• covered first with unchanged skin, which then acquires a characteristic red-violet or brown color above the compaction itself.

After some time, new nodules appear near the primary nodes, the foot swells, enlarges, looks deformed - its shape becomes ugly, like the foot of a mythical lizard with numerous warts. The nodes “mature” into abscesses, the wall of which ruptures after some time, and they open. And although the nodes are superficial, the resulting fistula tracts go deep, which indicates deep damage by infiltration of the tissues of the foot. From the fistulas flows purulent (sometimes mixed with blood) fluid with drusen, often with a characteristic disgusting odor.

Slow but steady progress of the process is observed, and over time the entire sole becomes covered with disfiguring nodes. They are not subjectively disturbing, as they are practically painless. Sometimes the sole becomes deformed so that the toes turn upward. Having filled the entire surface of the sole, nodules begin to appear on the dorsum of the foot. The deformation progresses to such an extent that the foot does not look like an anatomical structure, but like an ugly mass covered with pigment spots, in which many fistulous tracts and cavities are revealed, formed in place of the nodes after tissue decay.

The process does not stop and can spread deeper into muscle mass, tendons and bones. In some cases, atrophic changes in the lower leg muscles are noted. The appearance of the limb with Madura foot is characteristic and terrifying - a thin lower leg and a swollen, deformed foot.

As a rule, mycetoma affects only one foot. The disease itself can last a long time, years and even decades (on average from 10 to 20 years).

Diagnostics

If the process has gone far, up to the formation of fistulas and characteristic changes in the skin around them, diagnosing actinomycosis is not difficult. The initial stages of the development of the disease without additional research methods are much more difficult to determine.

The most reliable diagnostic result is the identification of radiant fungus microbiologically V:

• purulent contents from fistulas;
• tissue particles taken for analysis by biopsy;
• drusen (sometimes only threads of mycelium can be found in them).

For analysis for the purpose of bacteriological confirmation of actinomycosis, biological material is used - this is:

• purulent discharge from fistulous tracts;
• sputum (bronchial secretions);
• (in particular, from infiltrates).

To avoid erroneous diagnosis during the collection of biological material, one must be careful not to contaminate the samples with congenital actinomycotic saprophytic microflora from the mucous membranes. For this purpose, biological material (pus or tissue) is obtained in all possible cases:

• with percutaneous puncture;
• to diagnose the thoracic form of actinomycosis - through transtracheal puncture.

Such punctures, bypassing congenital foci of actinomycosis, are often the only way to obtain satisfactory samples of biological material for diagnostic research. But it should be remembered that when using biomaterial taken through transtracheal puncture, the diagnosis may also be unreliable, because the contents of the oral cavity, in which actinomycetes (both saprophytic and pathogenic) live, can enter the bronchi.

Actinomycetes are characterized by the ability to ferment, so they are easily subject to oxidation (although less than anaerobes). This means that it is necessary to transport biological material after collection to a bacteriological laboratory promptly, before it undergoes changes that can distort the results of the study and affect the diagnosis. If long-term transportation is still necessary, then it is necessary to use special media designed for transportation - like Stewart's medium.

The presence of drusen allows a preliminary diagnosis of actinomycosis to be made. They can be identified by examining an actinomycotic granule under a microscope placed on a cover glass with the addition of methylene blue dye. Antimycotic drusen are visualized as cauliflower-shaped particles in which:

• the center is not painted;
• the periphery is colored blue.

In these particles, leukocytes and mycelial threads are visible (in some cases with characteristic flasks painted pink), which diverge from the center of the granule to its periphery. The benefit of microbiological research lies in the fact that, in addition to actinomycetes, the accompanying microflora is determined in the smear, thanks to which concomitant infectious diseases can be correctly assessed.

You can isolate a culture of radiant fungus by sowing the material on the so-called Saburov’s medium. When sowing crops, the first results are obtained in 2-3 days. In these terms, characteristic spider-like microcolonies of Actinomyces israelii or Actinomyces gerencseriae can be visualized under the microscope.

When identifying different types of actinomycetes in a granule, the detection of specific antibodies, which is carried out using immunofluorescence, will help:

• straight;
• indirect.

This method allows you to determine different types of pathogens even without sowing cultures.

In some cases, for diagnostic purposes, an intradermal form with actinolysate is used (it is positive in 80% of all patients). In this case, only positive and sharply positive results– weakly positive ones are often observed in patients of dental clinics (for example, with alveolar pyorrhea, manifested by the discharge of pus from the alveoli). On the other side, a negative test does not mean the absence of actinomycosis. It is determined by:

• patients suffering from severe forms of this disease; negative result the test is explained by a significant and sudden suppression of cellular immunity;
• (in this case, a negative result will always be observed).

In many cases, actinomycosis, developing quickly, requires detailing in a short time. For the sake of faster diagnosis, molecular methods such as:

• genetic research;
• polymerase chain reaction ().

In some cases, the diagnosis is complicated due to the fact that:

• clinical symptoms are more typical for other diseases than for actinomycosis;
• (tissue examination) and serological (antibody determination) studies are low specific and low sensitivity . In other words, they can be positive not only for actinomycosis, but also for other diseases - on the other hand, for actinomycosis they give rather weak results, and this casts doubt on the fact that the disease is provoked specifically by the radiant fungus.

Detection of drusen is not 100% certain precise method when diagnosing actinomycosis: drusen contained only 25% of samples secreted from fistulas; their absence did not mean the absence of actinomycosis, which in these cases was confirmed using other diagnostic methods.

Instrumental diagnostic methods, which can be used to determine the presence of abscesses, act as auxiliary, because the detection of abscesses does not mean that they are of actinomycotic origin. On the other hand, instrumental methods can be an important aid in diagnosis if, due to the anatomical specifics, it is difficult to collect pus or perform a tissue biopsy. Thus, in case of actinomycosis, the central nervous system is examined with contrast, and the abscesses are visualized in the form of foci with the following characteristics:

• round or irregular in shape;
• with reduced density;
• surrounded by shadows in the form of wide rings.

Differential diagnosis

Pulmonary actinomycosis must be differentiated from:

• lung tumors;
• ulcers of the chest organs;
• other mycoses (primarily aspergillosis, nocardiosis, histoplasmosis - previously rare, now more common diseases);
• lung lesions.

Abdominal actinomycosis must be distinguished from surgical diseases:

• acute;
• local;
• diffuse peritonitis.

Actinomycosis of other organs and systems (joints, bones, kidneys, genitals, etc.) should be distinguished from their nonspecific purulent diseases.

Treatment

For the treatment of actinomycosis, a combination is used:

• etiotropic therapy - that is, aimed at the cause of the disease (antibacterial agents);
• immunotherapy.

– long-term, for 1-3 months. Apply:

• penicillins;
• tetracycline drugs.

These drugs have a good effect on radiant fungus; strains of actinomycetes insensitive to them have not been isolated.

For this purpose, actinolysate is used, which:

• stimulates the phagocytic process (“eating” foreign cells by phagocyte cells);
• enhances the production of antibodies to wide range microorganisms; this is valuable in case of multi-infection.

Surgical treatment is used to eliminate ulcers. Abscesses and a focus of empyema (a diffuse purulent lesion of tissue without walls, like an abscess) are opened and drained. If actinomycosis has led to massive damage to the lung tissue and its purulent melting, a lobectomy is performed (removal of the affected lobe of the lung).

Since relapses are possible, convalescents (cured people who no longer show signs of the disease) should remain under dispensary observation for a long time - from 6 to 12 months .

Prevention

There is no specific prevention of actinomycosis, no vaccines have been developed. If an outbreak is detected, no specific measures are taken.

Nonspecific prevention includes a number of fairly simple measures that protect not only from actinomycosis pathogens:

• thorough oral hygiene;
• timely visits to the dentist not only for therapeutic purposes, but also for preventive purposes, detection of the smallest dental problems and elimination of them;
• timely treatment of inflammatory changes in the oral mucosa and tonsils, prevention of tonsillitis.

Forecast

Without etiotropic therapy, the prognosis for health and life is unfavorable.