Pediatric Actinomycosis 

  • Author: Jorge M Quinonez, MD; Chief Editor: Russell W Steele, MD   more...
 
Updated: Nov 28, 2011
 

Background

Actinomycosis is a chronic bacterial disease. Localized swelling with suppuration, abscess formation, tissue fibrosis, and draining sinuses characterize this disease. Gram-positive, pleomorphic non–spore-forming, non–acid-fast anaerobic or microaerophilic bacilli of the genus Actinomyces and the order Actinomycetales cause actinomycosis. Actinomyces are very closely related to Nocardia species; both were once considered to be fungal organisms.

Infections of the oral and cervicofacial regions are the most commonly recognized infections; however, the thoracic region, abdominopelvic region, and the CNS are also frequently involved. Actinomyces israelii, Actinomyces naeslundii, Actinomyces odontolyticus, Actinomyces viscosus, and Actinomyces meyeri most frequently cause human actinomycosis. Actinomyces gerencseriae may also cause disease in humans. Three former Centers for Disease Control and Prevention (CDC) coryneform bacteria now have been added to the Actinomyces group and are thought to be potential causes for disease; these include Actinomyces neuii,[1] Actinomyces radingae, and Actinomyces turicensis. Actinomyces radicidentis, a recently described species, has been isolated with polymerase chain reaction from patients with endodontic infections.[2]

Actinomyces species grow well in enriched media with brain-heart infusion and may be aided in growth by an atmosphere of 6-10% ambient carbon dioxide. They grow best at 37°C. Colonies can appear at 3-7 days, but, to ensure that no growth is missed, observe cultures for 21 days.

Propionibacterium propionicus and related species of bacteria can also cause actinomycosislike disease. Other bacteria that are frequently isolated from clinical specimens concomitantly with Actinomyces in human infection include Actinobacillus actinomycetemcomitans, Eikenella corrodens, and species of Fusobacterium, Bacteroides, Capnocytophaga, Staphylococcus, Streptococcus, and Enterococcus.

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Pathophysiology

Actinomyces species that cause human disease are not found in nature but are normal flora of the oropharynx, GI tract, and female genital tract. This is not an exogenous infection; therefore, no person-to-person spread of the pathogen occurs.

In general, Actinomyces species, being members of the normal flora, are agents of low pathogenicity and require disruption of the mucosal barrier to cause disease. Oral and cervicofacial diseases are commonly associated with dental procedures, trauma, oral surgery, or dental sepsis. Pulmonary infections usually arise after aspiration of oropharyngeal or GI secretions. GI infection frequently follows loss of mucosal integrity, such as with surgery, appendicitis, diverticulitis, trauma, or foreign bodies. Numerous reports have linked the use of intrauterine contraceptive devices to the development of actinomycosis of the female genital tract.[3] The presence of a foreign body in this setting appears to trigger infection.

Other bacterial species that often are copathogens to Actinomyces species may aid spread of infection by inhibiting host defenses and reducing local oxygen tension. Once the organism is established locally, it spreads to surrounding tissues in a progressive manner, leading to a chronic, indurated, suppurative infection often with draining sinuses and fibrosis. In tissues, Actinomyces grow in microscopic or macroscopic clusters of tangled filaments surrounded by neutrophils. When visible, these clusters are pale yellow and exude through sinus tracts; they are called sulfur granules. This is not an exclusive finding of actinomycosis, and its absence does not rule out the diagnosis. Other conditions, such as eumycetoma and nocardiosis, have been linked to the production of sulfur granules.

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Epidemiology

Frequency

United States

The disease is uncommon. Studies in the Cleveland area in the 1970s showed incidence to be about 1 per 300,000 persons.

International

Studies in Germany and the Netherlands in the 1960s showed incidence of 1 per 100,000 persons. No data are available on the incidence of disease in developing nations.

Sex

A male-to-female infection ratio of 3:1 is encountered in most series. Unconfirmed explanations for this comprise poorer oral hygiene and augmented oral trauma in males.

Age

Infection can develop in individuals of all ages; however, it is rare in the pediatric population and in patients older than 60 years. Most cases are encountered in individuals in the mid decades of life.

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Contributor Information and Disclosures
Author

Jorge M Quinonez, MD  Senior Vice President and Chief Medical Officer, Family Health Centers of Southwest Florida, Inc

Jorge M Quinonez, MD is a member of the following medical societies: American Academy of Pediatrics and Infectious Diseases Society of America

Disclosure: Glaxo Smith Kline Consulting fee Speaking and teaching

Specialty Editor Board

Itzhak Brook, MD, MSc  Professor, Department of Pediatrics, Georgetown University School of Medicine

Itzhak Brook, MD, MSc is a member of the following medical societies: American Association for the Advancement of Science, American College of Physicians-American Society of Internal Medicine, American Federation for Clinical Research, American Medical Association, American Society for Microbiology, Armed Forces Infectious Diseases Society, Association of Military Surgeons of the US, Infectious Diseases Society of America, International Immunocompromised Host Society, International Society for Infectious Diseases, Medical Society of the District of Columbia, New York Academy of Sciences, Pediatric Infectious Diseases Society, Society for Ear, Nose and Throat Advances in Children, Society for Experimental Biology and Medicine, Society for Pediatric Research, Southern Medical Association, and Surgical Infection Society

Disclosure: Nothing to disclose.

Mary L Windle, PharmD  Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Mark R Schleiss, MD  American Legion Chair of Pediatrics, Professor of Pediatrics, Division Director, Division of Infectious Diseases and Immunology, Department of Pediatrics, University of Minnesota Medical School

Mark R Schleiss, MD is a member of the following medical societies: American Pediatric Society, Infectious Diseases Society of America, Pediatric Infectious Diseases Society, and Society for Pediatric Research

Disclosure: Nothing to disclose.

Robert W Tolan Jr, MD  Chief, Division of Allergy, Immunology and Infectious Diseases, The Children's Hospital at Saint Peter's University Hospital; Clinical Associate Professor of Pediatrics, Drexel University College of Medicine

Robert W Tolan Jr, MD is a member of the following medical societies: American Academy of Pediatrics, American Medical Association, American Society for Microbiology, American Society of Tropical Medicine and Hygiene, Infectious Diseases Society of America, Pediatric Infectious Diseases Society, Phi Beta Kappa, and Physicians for Social Responsibility

Disclosure: Novartis Honoraria Speaking and teaching

Chief Editor

Russell W Steele, MD  Head, Division of Pediatric Infectious Diseases, Ochsner Children's Health Center; Clinical Professor, Department of Pediatrics, Tulane University School of Medicine

Russell W Steele, MD is a member of the following medical societies: American Academy of Pediatrics, American Association of Immunologists, American Pediatric Society, American Society for Microbiology, Infectious Diseases Society of America, Louisiana State Medical Society, Pediatric Infectious Diseases Society, Society for Pediatric Research, and Southern Medical Association

Disclosure: Nothing to disclose.

References
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  2. Siqueira JF, Rocas IN. Polymerase chain reaction detection of Propionibacterium propionicus and Actynomyces radicidentis in primary and persistent endodontic infections. Oral Surg oral Med Oral Pathol Oral Radiol Endod. 2003;96:215-222. [Medline].

  3. Perlow JH, Wigton T, Yordan EL, et al. Disseminated pelvic actinomycosis presenting as metastatic carcinoma: association with the progestasert intrauterine device. Rev Infect Dis. Nov-Dec 1991;13(6):1115-9. [Medline].

  4. Kutluhan A, Salviz M, Yalçiner G, Kandemir O, Yesil C. The role of the actinomyces in obstructive tonsillar hypertrophy and recurrent tonsillitis in pediatric population. Int J Pediatr Otorhinolaryngol. Mar 2011;75(3):391-4. [Medline].

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  6. Cintron JR, Del Pino A, Duarte B, et al. Abdominal actinomycosis. Dis Colon Rectum. Jan 1996;39(1):105-8. [Medline].

  7. Henderson SR. Pelvic actinomycosis associated with an intrauterine device. Obstet Gynecol. May 1973;41(5):726-32. [Medline].

  8. Koshi G, Lalitha MK, Samraj T, et al. Brain abscess and other protean manifestations of actinomycosis. Am J Trop Med Hyg. Jan 1981;30(1):139-44. [Medline].

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  10. Robinson JL, Vaudry WL, Dobrovolsky W. Actinomycosis presenting as osteomyelitis in the pediatric population. Pediatr Infect Dis J. Apr 2005;24(4):365-9. [Medline].

  11. Russo T. Agents of Actinomycosis. In: Mandell G, Bennett J, Dolin R, eds. Principles and Practice of Infectious Diseases. 4th ed. New York, NY: Churchill Livingston; 1995:2280-8.

  12. Sakallioglu U, Acikgoz G, Kirtiloglu T, et al. Rare lesions of the oral cavity: case report of an actinomycotic lesion limited to the gingiva. J Oral Sci. Mar 2003;45(1):39-42. [Medline].

  13. Skoutelis A, Petrochilos J, Bassaris H. Successful treatment of thoracic actinomycosis with ceftriaxone. Clin Infect Dis. Jul 1994;19(1):161-2. [Medline].

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  15. Smego RA Jr, Foglia G. Actinomycosis. Clin Infect Dis. Jun 1998;26(6):1255-61; quiz 1262-3. [Medline].

  16. Snape PS. Thoracic actinomycosis: an unusual childhood infection. South Med J. Feb 1993;86(2):222-4. [Medline].

  17. Tanaka-Bandoh K, Watanabe K, Kato N, et al. Susceptibilities of Actinomyces species and Propionibacterium propionicus to antimicrobial agents. Clin Infect Dis. Sep 1997;25 Suppl 2:S262-3. [Medline].

  18. 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. Dec 1975;135(12):1562-8. [Medline].

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