Dermatologic Aspects of Actinomycosis Clinical Presentation

  • Author: Talib Najjar, DMD, MDS, PhD; Chief Editor: Dirk M Elston, MD   more...
 
Updated: May 23, 2012
 

History

Constitutional symptoms of actinomycosis may include nonspecific complaints such as weight loss, coughing, chest pain, and fever. When actinomycosis involves the jawbones, it is usually associated with localized pain, swelling, and draining fistulas. Actinomycosis may mimic other bacterial osteomyelitis.

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Physical

Consider actinomycosis infection in the differential diagnosis of any acute, subacute, or chronic cutaneous or soft tissue swelling of the face, head, or neck.

  • Presentations
    • The cervicofacial form of actinomycetes infection is the most common presentation of actinomycosis, occurring in 55% of patients.
    • GI ingestion of the organism leads to the abdominopelvic form, which affects approximately 20% of patients.
    • Tracheobronchial aspiration of the organism from the oral cavity leads to the pulmonothoracic presentation, which occurs in 15% of patients. Thoracic infection may involve the lungs, pleurae, mediastinum, or chest wall. The classic, chronic, chest wall sinus that discharges granules is uncommon today because antibiotics tend to limit infection to the lung.[14]
    • Other manifestations of actinomycosis include a pelvic form of actinomycosis that is associated with the use of intrauterine contraceptive devices.[11]
  • Findings
    • Acute or chronic signs of systemic infection may be absent. The patient's temperature may be in the reference range.
    • Hemoptysis is unusual in actinomycosis, but it can occur with a lung abscess.
    • Actinomycosis may present as a simple phlegmon; a draining sinus; or an abscess in the cheek, in the angle of the jaw, or in the submandibular region (see the image below). Diagram of potential oral anaerobic infection. Diagram of potential oral anaerobic infection.
    • The most common feature of actinomycosis infection is the presence of acute pyogenic infection in the submandibular or paramandibular area; in the angle of the mandible, maxilla, and palate; in the parotid region; or in the neck.
    • Primary infection in the skin of the face may spread to adjacent structures such as the scalp, orbit, ears, and other areas.
    • Oral infection may spread to the tongue, hypopharynx, larynx, trachea, salivary glands, and paranasal sinuses.[15]
    • Unlike other bacterial infections, actinomycosis spreads without regard for facial tissue planes and without adenopathy. Actinomycosis may mimic chronic but persistent osteomyelitis.
    • Actinomycosis infection in the jaw begins as a chronic tissue induration with trismus; ultimately, a draining cutaneous or oral fistula develops (see the image below). The fistula progresses to an acute suppurative infection with abscess formation beneath the skin and trismus, and the edema of the surrounding tissues is out of proportion to the degree of inflammation.[8] Image shows an oral fistula caused by actinomycosiImage shows an oral fistula caused by actinomycosis.
    • Infection inside the oral cavity can present as an acute abscess, a subacute inflammatory nodule, an infiltrating mass, or a pseudotumor. It may not respond to initial antibiotic and conservative surgical manipulation.
    • Persistent infection in the periapical area of the tooth, especially in the premolar and molar region, may harbor actinomycetes, which can lead to the development of an oral or skin sinus fistula (see the image below). Periapical radiograph shows infection in the premoPeriapical radiograph shows infection in the premolar tooth.
  • Primary long bone infection is rare. Osseous involvement in actinomycosis is derived from adjacent soft tissue infection, provoking a painful periostitis that results in new bone formation at the site of infection, which can be seen at radiography (see Imaging Studies). The mandible is 4 times more commonly involved than the maxilla.[16]
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Causes

The pathogen in actinomycosis is a filamentous bacterium in the genus Actinomyces. Usually, actinomycosis is caused by A israelii, an anaerobic gram-positive organism that enters the tissue through a break in the mucosa.[2] All are oral facultative or anaerobic gram-positive commensal organisms, equally capable of producing lesions consistent with actinomycosis.

Actinomyces species are prevalent in the oral cavity. The bacteria are isolated from the interdental sulci, periodontal membranes, tonsillar crypts, and saliva.[12] Poor oral hygiene and dental caries appear to be primary predisposing conditions for the development of actinomycosis. In addition, the presence of associated bacteria appears to be fundamental to the development of clinical infection (see Lab Studies).

Currently, 4 species are recognized in actinomycosis. In order of importance, they are A israelii, Actinomyces naeslundii, Actinomyces viscosus, and Actinomyces odontolyticus.[1]

  • A israelii grows best in anaerobic conditions; many strains are microaerophilic, and some grow after prolonged anaerobic incubation in carbon dioxide.[14]
    • Another characteristic feature of the bacteria is the formation of mature colonies (within 5-10 d), which are large, white, opaque, rough looking, and heaped up or lobulated (molar-tooth appearance).
    • In early or acute actinomycosis, the organisms may appear as free gram-positive filaments.
    • In advanced lesions, characteristic sulfur granules are usually found (see the image below).Photomicrograph of a characteristic sulfur granulePhotomicrograph of a characteristic sulfur granule of actinomycosis (hematoxylin and eosin, original magnification X10).
    • Other characteristic features of this organism are the production of leukotoxin and the presence of a bone resorption endotoxin, a polymorphonuclear neutrophil chemotaxis inhibitor, and a lipopolysaccharide endotoxin.
  • A naeslundii is most commonly found in blood, brain tissue, and other abscesses.
    • These organisms have also been found in cervicofacial infections, gallbladder empyema, suppurative thyroiditis, pleural empyema, pelvic infection related to intrauterine devices, and mycotic aneurysms in the splenic artery.
    • The pathogen of grows well in aerobic and anaerobic conditions, but it is considered facultative only in the presence of carbon dioxide.[12]
  • A viscosus specifically produces catalase and grows well in aerobic conditions, with or without added carbon dioxide.
    • This is a common organism in dental plaque.[13]
    • It is probably an agent of periodontal disease.[13]
    • This organism may cause various pulmonary and cervicofacial infections, as well as bacteremia and endocarditis.[13]
  • A odontolyticus has been associated with all major forms of actinomycosis, including septicemia and disseminated liver abscesses.[17]
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Contributor Information and Disclosures
Author

Talib Najjar, DMD, MDS, PhD  Professor of Oral and Maxillofacial Surgery and Pathology, University of Medicine and Dentistry of New Jersey

Talib Najjar, DMD, MDS, PhD is a member of the following medical societies: American Society for Clinical Pathology

Disclosure: Nothing to disclose.

Specialty Editor Board

Janet Fairley, MD  Professor and Head, Department of Dermatology, University of Iowa, Roy J and Lucille A Carver College of Medicine

Janet Fairley, MD is a member of the following medical societies: American Academy of Dermatology, American Dermatological Association, American Federation for Medical Research, and Society for Investigative Dermatology

Disclosure: Nothing to disclose.

Michael J Wells, MD  Associate Professor, Department of Dermatology, Texas Tech University Health Sciences Center, Paul L Foster School of Medicine

Michael J Wells, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, and Texas Medical Association

Disclosure: Nothing to disclose.

Drore Eisen, MD, DDS  Consulting Staff, Department of Dermatology, Dermatology Research Associates of Cincinnati

Drore Eisen, MD, DDS is a member of the following medical societies: American Academy of Dermatology, American Academy of Oral Medicine, and American Dental Association

Disclosure: Nothing to disclose.

Catherine M Quirk, MD  Clinical Assistant Professor, Department of Dermatology, University of Pennsylvania

Catherine M Quirk, MD is a member of the following medical societies: Alpha Omega Alpha and American Academy of Dermatology

Disclosure: Nothing to disclose.

Chief Editor

Dirk M Elston, MD  Director, Ackerman Academy of Dermatopathology, New York

Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology

Disclosure: Nothing to disclose.

Additional Contributors

Many thanks for continuous help and advice from doctor Edward Jonson, MD, internationally known infectious diseases specialist and Dean, Trinity School of Medicine and Caribbean Studies, Saint Vincent.

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Photomicrograph of gram-positive organisms in actinomycosis, which may be confused with those causing a mycotic infection (hematoxylin and eosin, original magnification X40).
Photomicrograph of a characteristic sulfur granule of actinomycosis (hematoxylin and eosin, original magnification X10).
Diagram of potential oral anaerobic infection.
Image shows an oral fistula caused by actinomycosis.
Periapical radiograph shows infection in the premolar tooth.
 
 
 
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