Overview.
Chronic pyogenic granulomatous disease caused by Actinomyces. The lesions occur in the face, neck, chest and abdomen, and are characterized by expansion into the surrounding tissues to form fistulas and discharge pus with sulfur-like particles. High-dose, long course of penicillin treatment is effective in most cases, and tetracycline, erythromycin, lincomycin and cephalosporin antibiotics can also be used; at the same time, it is also necessary to surgically drain the pus and surgical resection of fistula. This disease is not infectious, pay attention to oral hygiene can prevent this disease.
Pathogenesis
The most common pathogen is Actinobacillus israelii. These pathogenic bacteria are anaerobic or slightly aerobic, often a normal flora in the body, especially in the oral cavity is often seen. Infection can occur after surgery if there is trauma. The infection is often combined with bacterial infections, and the damage gradually spreads from the center to the periphery through sinus tracts, invading the skin, subcutaneous tissues, muscles, fascia, bones, and internal organs. It can be spread through the digestive tract and trachea, and rarely through bloodstream.
Symptoms
1. Actinomycosis of face and neck
It is the most common and may develop first by parasitizing in the mouth. Pathogenic bacteria can be invaded by dental caries or periodontal abscess, tonsil foci, etc., preferably in the face and neck junction, the surface of the skin is dark red or brownish-red, and later form abscesses, local plate-like hardness, the abscesses are pierced into a number of pus-discharging sinusoids, and pus is commonly discharged in the “sulfur particles”. The lesion can be extended to the skull, neck, shoulder and chest, etc., and when it affects the masticatory muscles, it can cause the teeth to close, and in the later stage, it can cause periostitis and osteomyelitis underneath it.
2. Abdominal actinomycosis
Pathogenic bacteria swallowed by the oral cavity invade the intestinal mucosa and cause the disease, but also can be directly affected by the chest lesions. Prevalent in the ileocecal region, such as acute, subacute or chronic appendicitis manifestations, local mass plate-like hardness, and then penetrate the abdominal wall into a fistula, pus can be seen in the “sulfur particles”, can be accompanied by fever, night sweats, malaise, emaciation, and other systemic symptoms, but also to other abdominal organs, such as the stomach, liver, kidneys, etc., or spread to the spine, ovary, bladder, chest, or blood dissemination of invasion of the middle and middle parts of the body, or blood dissemination. It may also spread to the spine, ovaries, bladder, chest cavity, or invade the central nervous system by hematogenous dissemination.
3. Chest actinomycosis
Pathogenic bacteria enter the lungs through the respiratory tract and cause the disease, and can also be directly affected by the adjacent Department of Actinomycosis, often invading the lung hilum or lung base, presenting acute or chronic infection manifestations, such as irregular fever, chest pain, cough, coughing up sputum with blood, night sweats, emaciation and so on. Involvement of pleura can lead to pleuritis, pus chest, can form pus drainage fistula, pus in the “sulfur particles”, X-ray shows solid changes in the lung lobes, which can have translucent areas, can be accompanied by pleural adhesions and pleural effusion, can also be spread to the pericardium to cause pericarditis.
4. Cerebral actinomycosis
(1) Limited type, including thick-walled abscesses and granulomas, is mostly found in the brain, and can also involve the third ventricle and the posterior fossa, causing elevated cranial pressure. Cerebral nerve involvement may cause headache, nausea, vomiting, diplopia, optic disc hemorrhage, etc.
(2) Diffuse type: simple meningitis or brain abscess, but also epidural abscess and cranial osteomyelitis.
5. Cutaneous actinomycosis
Actinomycosis is caused by direct skin contact with pathogenic bacteria and can be located in various parts of the body. Initially subcutaneous nodules, softened and broken into sinus tracts, can be extended to the surrounding area, satellite subcutaneous nodules. Broken into a fistula, pus in the “sulfur particles”. The disease is chronic. It may also invade deeper tissues and become hard due to fibrosis and scarring.
Examination
1. Pathogenic bacteria examination
(1) Direct microscopic examination: Gram staining of granules, blue mycelial clusters and rods can be seen. Pus smears may also find fine and short branched-like hyphae that stain negatively for antacid. Note the positive antacid staining of Nucella, and the sporulation of Streptococcus.
(2) Cultivation More difficult, particles must be washed several times with sterile saline to remove bacteria, then crushed with a sterilized glass rod and inoculated on blood agar of brain-heart infusion by delineation to a CO2 anaerobic vat at 37℃.
2.Histopathology
Early localized leukocyte infiltration, the formation of small abscesses, penetration of the formation of sinus tracts, the sinus tracts can be intercommunicated. The body fascia, pleura, diaphragm, bone, etc. can not prevent its development. There may be chronic granulomatous tissue proliferation near the purulent area, infiltration of lymphoid cells, plasma cells, histiocytes and fibroblasts, etc. The local tissues may be vitreous degeneration, resulting in sclerotinia, and sulfur granules can be seen in the abscess, and the central part of HE staining is homogeneous, with fenestrated short rod-like cells around it.
Diagnosis
Typical clinical presentation, special imaging findings, and sulfur granules found in the pus, the diagnosis is not difficult. In addition, the diagnosis can be further confirmed by combining with pathogenetic examination and histopathology.
Treatment
1. Systemic treatment
High dose and long course penicillin treatment is effective for this disease, intramuscular or intravenous, other such as lincomycin, tetracycline, chloramphenicol, streptomycin, sulfonamides, rifampicin and so on also have a certain degree of efficacy. Polyenes and azoles and other antifungal agents are ineffective for this disease.
2. Local treatment
All superficial lesions and sinus abscesses should be excised or incised and drained.