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. 
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.  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.  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.  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.  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.  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. 
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. 
The incidence of human actinomycosis has been decreasing in the United States. Weese and Smith  reported prevalences of 1 case per 12,000 admissions in the 1930s and 1 case per 21,000 admissions in the 1950s. Bennhoff  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. 
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.  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.
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