Dermatologic Aspects of Actinomycosis

Dermatologic Aspects of Actinomycosis

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Many infectious and inflammatory diseases affect the skin and the oral mucosa. Actinomycosis is one such characteristic and persistent infection. Actinomycosis is a subacute, chronic, cellulitic invasion of the soft tissues that causes the formation of external sinus tracts that discharge sulfur granules. This process spreads unimpeded by traditional anatomic barriers after the endogenous oral commensal organisms invade the tissues of the face and neck. [1, 2, 3] Actinomycosis may also spread to the pulmonary and GI systems. [4]

Actinomycosis is caused by various bacterial species of the actinomycete group. Usually, the disease is caused by Actinomyces israelii, an anaerobic gram-positive organism that enters the tissue through a break in the mucosa. [5] The Actinomyces genus of bacteria includes other species that normally inhabit the oral cavity but are seldom pathogenic. Actinomycosis begins as an inflammatory soft tissue mass, which can enlarge into an abscesslike swelling, with penetration of the overlying skin and the development of recognizable draining fistulae.

The term actinomycosis is misleading. Because of the derivative term mycosis (from the Greek mykes), some believe that actinomycosis is a fungal infection, although it is not a fungal infection. Aktino referred to the radiating organism in the sulfur granule as ray fungus. Human actinomycosis was first described in the medical literature in 1857, although a similar disease in cattle had been described in 1826. In 1877, Bollinger found Actinomyces bovis in granules from cattle with a condition called lumpy jaw. In 1878, Israel discovered granules in human autopsy material and described actinomycosis in humans in 1885. [6] Israel further discovered that Actinomyces species do not survive outside mammalian hosts and that they are not found exogenously in plants or soil.

Prior to the antibiotic era, actinomycosis was a common illness and easily recognized at clinical examination. However, the microbiologic features of the etiologic organisms were not fully clarified until the 1940s. [7] The therapeutic outcome of surgical management was variable, and even if healing occurred, sequelae and complications were common. [8, 9] Actinomycosis often became lifelong, and death was not unusual. At the dawn of the antibiotic era, morbidity resulting from actinomycosis decreased, and a general lack of familiarity with the disease process resulted. [10] Subsequently, diagnoses of actinomycosis were often delayed because of a lack of microbiologic techniques.

The article Bacterial Mouth Infections also may be of interest.

The pathogen is in actinomycosis a filamentous bacterium (see the image below and Causes). Historically, actinomycosis has been confused with a fungal disease because of its appearance and the slowly progressive nature of the lesions, which mimics mycotic illness. Confusion was so great that, for many years, some investigators placed Actinomyces species in an intermediate status between fungi and bacteria. [5] The unique nature of the organism is the absence of a nuclear membrane, which places Actinomyces species among the higher prokaryotic bacteria. The lack of chitin and gluten, coupled with the presence of muramic acid in the cell walls and the absence of mitochondria, is another distinct feature. [11]

All species of Actinomyces are normal commensal inhabitants of the oral and buccal cavities in humans and certain other mammals. They cannot be classified as symbiotic organisms because they do not have a mutually beneficial relationship with their host. They are not true parasites because they usually do not cause harm to the host; however, they definitely assume a parasitic role when they result in an infection with an inflammatory tissue response. Similar to Mycobacterium tuberculosis, actinomycetes survive phagocytosis by host cells, and they may be characterized as facultative intracellular parasites.

Actinomycosis does not appear to be an opportunistic infection because actinomycosis is not common in patients who are immunosuppressed or in patients with AIDS. One of the authors has experience in producing a bone infection in animals that leads to osteomyelitis; however, actinomycosis could not be induced in the tibias and mandibles of rabbits. This outcome may have been the result of the avirulent nature of the organisms. Perhaps the presence of other infectious bacteria is required in addition to the Actinomyces species to initiate the infection in experimental models. [12]

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. [5] 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. [13] 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. [4]

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). 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. [13]  

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. [15]  It is probably an agent of periodontal disease. [15]  This organism may cause various pulmonary and cervicofacial infections, as well as bacteremia and endocarditis. [15]

A odontolyticus has been associated with all major forms of actinomycosis, including septicemia and disseminated liver abscesses. [16]

United States

The incidence of human actinomycosis has been decreasing in the United States. Weese and Smith [17] reported prevalences of 1 case per 12,000 admissions in the 1930s and 1 case per 21,000 admissions in the 1950s. Bennhoff [18] reported a prevalence of only 1 case per 63,000 admissions in the 1970s. Actinomycosis can still be found in inner-city populations of the United States.


Actinomycosis remains a problem in underdeveloped countries. [13]

Actinomycosis affects persons of all socioeconomic levels and all races, and actinomycosis is not limited to any single segment of the population.

A male-to-female predominance in a ratio of approximately 3:1 has been observed for actinomycosis. [15] This predominance is postulated to reflect the greater likelihood for facial and oral trauma and the lack of oral hygiene in males compared with females.

The incidence of actinomycosis is higher in persons aged 30-60 years than in others, and actinomycosis is rare in children. This difference may reflect the increased incidence of periodontal disease in elderly individuals.

Antibiotics modify the natural course of actinomycosis, reduce complications, and improve survival. With the combined use of penicillin and surgery, cure for actinomycosis has become the rule rather than the exception. Cervicofacial infection, if recognized early, has an excellent prognosis with the use of antibiotics alone. No evidence of long-term morbidity is observed in patients with actinomycosis treated with antibiotics and surgical excision of the necrotic tissue.

Nordqvist C. What is Actinomycosis? What causes Actinomycosis?. Medical News Today. Available at May 8, 2012; Accessed: June 14, 2016.

Martín-Cabrejas BM, Gargantilla-Madera P, Pintor-Holguin E. Cervicofacial Actinomycosis. J Fam Med Dis Prevent. 2016. 2(1):[Full Text].

Könönen E, Wade WG. Actinomyces and related organisms in human infections. Clin Microbiol Rev. 2015 Apr. 28 (2):419-42. [Medline].

Schaal KP, Schofield GM. Classification and identification of clinically significant Actinomycetaceae. Ortiz-Ortiz L, Bojalil LF, Yakoleff V, eds. Biological, Biochemical, and Biomedical Aspects of Actinomycetes. Orlando, Fla: Academic Press; 1984. 505-20.

Eastridge CE, Prather JR, Hughes FA Jr, Young JM, McCaughan JJ Jr. Actinomycosis: a 24 year experience. South Med J. 1972 Jul. 65(7):839-43. [Medline].

Richtsmeier WJ, Johns ME. Actinomycosis of the head and neck. CRC Crit Rev Clin Lab Sci. 1979 Nov. 11(2):175-202. [Medline].

Erikson D. Pathogenic anaerobic organisms of the Actinomyces group. Br Med Res Council Special Report Series. 1940. 240:1.

Waksman SA, Henrici AT. The Nomenclature and Classification of the Actinomycetes. J Bacteriol. 1943 Oct. 46(4):337-41. [Medline].

Georg LK. The agents of human actinomycosis. Balows A, Dehau RM, Dowell VR, eds. Anaerobic Bacteria: Role in Disease. Springfield, Ill: Charles C Thomas; 1974. 237-56.

Brock DW, Georg LK, Brown JM, Hicklin MD. Actinomycosis caused by Arachnia propionica: report of 11 cases. Am J Clin Pathol. 1973 Jan. 59(1):66-77. [Medline].

Behbehani MJ, Heeley JD, Jordan HV. Comparative histopathology of lesions produced by Actinomyces israelii, Actinomyces naeslundii, and Actinomyces viscosus in mice. Am J Pathol. 1983 Mar. 110(3):267-74. [Medline].

Najjar TA, McKeon J, Smith L, Parson R. Septic arthritis of TMJ secondary to experimental osteosynthesis. J Dent Res. 1980. 59A:306.

Coleman RM, Georg LK, Rozzell AR. Actinomyces naeslundii as an agent of human actinomycosis. Appl Microbiol. 1969 Sep. 18(3):420-6. [Medline].

Pine L, Overman JR. Determination of the structure and composition of the “sulphur granules” of Actinomyces bovis. J Gen Microbiol. 1963 Aug. 32:209-23. [Medline].

Eng RH, Corrado ML, Cleri D, Cherubin C, Goldstein EJ. Infections caused by Actinomyces viscosus. Am J Clin Pathol. 1981 Jan. 75(1):113-6. [Medline].

Peloux Y, Raoult D, Chardon H, Escarguel JP. Actinomyces odontolyticus infections: review of six patients. J Infect. 1985 Sep. 11(2):125-9. [Medline].

Weese WC, Smith IM. A study of 57 cases of actinomycosis over a 36-year period. A diagnostic ‘failure’ with good prognosis after treatment. Arch Intern Med. 1975 Dec. 135(12):1562-8. [Medline].

Bennhoff DF. Actinomycosis: diagnostic and therapeutic considerations and a review of 32 cases. Laryngoscope. 1984 Sep. 94(9):1198-217. [Medline].

Thukral R, Shrivastav K, Mathur V, Barodiya A, Shrivastav S. Actinomyces: a deceptive infection of oral cavity. J Korean Assoc Oral Maxillofac Surg. 2017 Aug. 43 (4):282-285. [Medline].

Brown JR. Human actinomycosis. A study of 181 subjects. Hum Pathol. 1973 Sep. 4(3):319-30. [Medline].

Lewis RP, Sutter VL, Finegold SM. Bone infections involving anaerobic bacteria. Medicine (Baltimore). 1978 Jul. 57(4):279-305. [Medline].

Metgud SC. Primary cutaneous actinomycosis: a rare soft tissue infection. Indian J Med Microbiol. 2008 Apr-Jun. 26(2):184-6. [Medline].

Schaal KP, Beaman BL. Clinical significance of actinomycetes. Goodfellow M, Mordarski M, Williams S, eds. The Biology of the Actinomycetes. New York: Academic Press; 1983. 389-424.

Hennrikus EF, Pederson L. Disseminated actinomycosis. West J Med. 1987 Aug. 147(2):201-4. [Medline].

Lerner PI. Susceptibility of pathogenic actinomycetes to antimicrobial compounds. Antimicrob Agents Chemother. 1974 Mar. 5(3):302-9. [Medline].

Deshpande RB, Rao AA. Cervicofacial actinomycosis with upper cervical vertebral involvement and fatal meningitis (a case report). J Postgrad Med. 1985 Oct. 31(4):223-5. [Medline].

Sezer B. Established prolonged antimicrobial treatment regimens against actinomycosis. Amer Assoc of OMFS (Position Paper). 2017.

Holmberg K, Nord CE, Dornbusch K. Antimicrobial in vitro susceptibility of actinomyces israelii and arachnia propionica. Scand J Infect Dis. 1977. 9(1):40-5. [Medline].

Boand A, Novak M. Sensitivity changes of Actinomyces bovis to penicillin and streptomycin. J Bacteriol. 1949 May. 57(5):501-8. [Medline].

Edelmann M, Cullmann W, Nowak KH, Kozuschek W. Treatment of abdominothoracic actinomycosis with imipenem. Eur J Clin Microbiol. 1987 Apr. 6(2):194-5. [Medline].

Steininger C, Willinger B. Resistance patterns in clinical isolates of pathogenic Actinomyces species. J Antimicrob Chemother. 2016 Feb. 71 (2):422-7. [Medline].

Jeong YJ, Suh HW, Shim HS. Cervicofacial Primary Cutaneous Actinomycosis: Surgical Treatment for Complete Remission of the Disease. J Craniofac Surg. 2017 May. 28 (3):e269-e271. [Medline].

Talib Najjar, DMD, MDS, PhD Professor of Oral and Maxillofacial Surgery and Pathology, Rutgers School of Dental Medicine

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

Disclosure: Nothing to disclose.

Michael J Wells, MD, FAAD Dermatologic/Mohs Surgeon, The Surgery Center at Plano Dermatology

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

Disclosure: Nothing to disclose.

Drore Eisen, MD, DDS Consulting Staff, Dermatology of Southwest Ohio

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

Disclosure: Nothing to disclose.

Dirk M Elston, MD Professor and Chairman, Department of Dermatology and Dermatologic Surgery, Medical University of South Carolina College of Medicine

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

Disclosure: Nothing to disclose.

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 Federation for Medical Research, Society for Investigative Dermatology

Disclosure: Nothing to disclose.

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.

Dermatologic Aspects of Actinomycosis

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