Actinomycosis
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Aditya Ganti M.B.B.S. [2]
Synonyms and keywords: Actinomyces infection; Actinomyces israelii infection; Lumpy jaw;
Overview
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Aditya Ganti M.B.B.S. [2]
Overview
Actinomycosis is a rare infectious bacterial disease of humans generally caused by Actinomyces israelii, A. gerencseriae and Propionibacterium propionicus. It is characterized by formation of painful abscesses in mouth, lungs, and digestive organs. The abscesses tend to grow larger as the disease progresses. In such conditions, the abscesses may penetrate the surrounding bone, muscle and skin, forming a sinus tract leaking large amounts of pus. Actinomycosis is also seen in cattle and is known as lumpy jaw. as the abscesses tend to grow on the head and neck of the animal.
Historical Perspective
Acitnomycosis was first discovered in 1877 in cattle by pathologist Otto Bollinger. Later in the same year, James Israel discovered it in humans and classified it under fungal origin. In 1939, Bergey classified to be bacteria.
Classification
Actinomycosis can be classified based on the anatomical site involved into[1]
- Orocervicofacial actinomycosis
- Thoracic actinomycosis
- Abdominopelvic actinomycosis
- Central nervous system actinomycosis
- Musculoskeletal actinomycosis
- Disseminated actinomycosis
Pathophysiology
Actinomycosis is a chronic pyogenic bacterial infection caused by Actinomyces species. Infection most frequently follows dental work, trauma and surgery. When there is break in the mucosal layer, anywhere from the mouth to the rectum they reach tissues and cause damage. Incubation period of actinomycosis varies from one to four weeks. But occasionally, it may be as long as several months. Actinomycosis elicits both humoral and cell-mediated immune responses.[2][3][4][5][6][7]
Causes
Actinomyces is a genus of Gram-positive bacteria. Some species are anaerobic, while others are facultatively anaerobic. Actinomyces species do not form spores, and, while individual bacteria are rod-shaped, morphologically Actinomyces colonies form fungus-like branched networks of hyphae. Many actinomyces species are opportunistic pathogens of humans and other mammals, particularly in the oral cavity. In rare cases, these bacteria can cause actinomycosis, a disease characterized by the formation of abscesses in the mouth, lungs, or the gastrointestinal tract.[8][9][10]
Differentiating Actinomycosis from other diseases
The differential diagnosis of actinomycosis consists of blastomycosis, brain abscess, colon cancer, crohn disease, diverticulitis, liver abscess, lung abscess, lymphoma, nocardiosis, pelvic inflammatory disease, pneumonia, tuberculosis and uterine cancer.
Epidemiology and Demographics
In 1970, its annual incidence was estimated to be 1 per 300,000. Its incidence has been declined due the advent of widespread use of antibiotics following dental surgeries. Actinomycosis is commonly found between 4th to 6th decade of life and very rare in infants and children. Males are more commonly affected by actinomycosis than females.
Risk factors
Common risk factors in the development of actinomycosis include dental abscess, oral surgery, and facial trauma.
Screening
According to the Centers for disease control and prevention, screening for actinomycosis is not recommended.
Natural history, Complications and Prognosis
If left untreated, patients with actinomycosis may progress to develop focal organ involvement with mass-like features and dvelopment of sinus tracts (which can heal and reform leading to multiple abscesses complications that can develop as a result of actinomycosis include local extension of disease resulting in osteomyelitis of the mandible, ribs, or vertebrae.The prognosis is generally excellent with prompt and effective antimicrobial treatment in patients in uncomplicated actinomycosis. Mortality range from 0% to 28%.[2][3][4][5][6][7][11]
Diagnosis
History and Symptoms
Actinomycosis can present with diverse clinical presentation, which include systemic flu-like symptoms and symptoms due to focal involvement of organs by the bacteria.[12][13][14][15][16][17][5]
Physical Examination
The physical examination findings of actinomycosis are mostly nonspecific and are described according to the organ involved [1]
Laboratory findings
The gold standard for diagnosing actinomycosis is histological examination and bacterial culture.[18][19]
Xray Chest
There are no specific chest X-ray findings for actinomycosis.
Treatment
Medical therapy
Antibiotics are the mainstay of treatment in actinomycosis. The exact antibiotic regimen depends on the site of infection, the severity of disease, and the patient’s response to treatment. For cervicofacial actinomycosis, Ampicillin is administered followed by Penicillin V. Patients with a more extensive disease requires surgery.
Surgery
Surgery is indicated when the disease involves chest, abdomen, pelvis, and central nervous system (CNS). Surgical resection is required for infected tissue with extensive necrosis and presence of multiple sinus tracts, or fistulas. It is also indicated if malignancy cannot be excluded or if large abscesses cannot be drained by percutaneous aspiration.
References
- ↑ 1.0 1.1 Valour F, Sénéchal A, Dupieux C, Karsenty J, Lustig S, Breton P, Gleizal A, Boussel L, Laurent F, Braun E, Chidiac C, Ader F, Ferry T (2014). “Actinomycosis: etiology, clinical features, diagnosis, treatment, and management”. Infect Drug Resist. 7: 183–97. doi:10.2147/IDR.S39601. PMC 4094581. PMID 25045274.
- ↑ 2.0 2.1 Volante M, Contucci AM, Fantoni M, Ricci R, Galli J (2005). “Cervicofacial actinomycosis: still a difficult differential diagnosis”. Acta Otorhinolaryngol Ital. 25 (2): 116–9. PMC 2639881. PMID 16116835.
- ↑ 3.0 3.1 Sharkawy AA (2007). “Cervicofacial actinomycosis and mandibular osteomyelitis”. Infect. Dis. Clin. North Am. 21 (2): 543–56, viii. doi:10.1016/j.idc.2007.03.007. PMID 17561082.
- ↑ 4.0 4.1 Peipert, Jeffrey F. (2004). “Actinomyces: Normal Flora or Pathogen?”. Obstetrics & Gynecology. 104 (Supplement): 1132–1133. doi:10.1097/01.AOG.0000145267.59208.e7. ISSN 0029-7844.
- ↑ 5.0 5.1 5.2 Higashi Y, Nakamura S, Ashizawa N, Oshima K, Tanaka A, Miyazaki T, Izumikawa K, Yanagihara K, Yamamoto Y, Miyazaki Y, Mukae H, Kohno S (2017). “Pulmonary Actinomycosis Mimicking Pulmonary Aspergilloma and a Brief Review of the Literature”. Intern. Med. 56 (4): 449–453. doi:10.2169/internalmedicine.56.7620. PMID 28202870.
- ↑ 6.0 6.1 Schaal KP, Lee HJ (1992). “Actinomycete infections in humans–a review”. Gene. 115 (1–2): 201–11. PMID 1612438.
- ↑ 7.0 7.1 Brown, James R. (1973). “Human actinomycosisA study of 181 subjects”. Human Pathology. 4 (3): 319–330. doi:10.1016/S0046-8177(73)80097-8. ISSN 0046-8177.
- ↑ Bowden GHW (1996). Actinomycosis in: Baron’s Medical Microbiology (Baron S et al, eds.) (4th ed. ed.). Univ of Texas Medical Branch. (via NCBI Bookshelf) ISBN 0-9631172-1-1.
- ↑ Holt JG (editor) (1994). Bergey’s Manual of Determinative Bacteriology (9th ed. ed.). Williams & Wilkins. ISBN 0-683-00603-7.
- ↑ Madigan M; Martinko J (editors). (2005). Brock Biology of Microorganisms (11th ed. ed.). Prentice Hall. ISBN 0-13-144329-1.
- ↑ Agrawal P, Vaiphei K (2014). “Renal actinomycosis”. BMJ Case Rep. 2014. doi:10.1136/bcr-2014-205892. PMC 4244330. PMID 25406215.
- ↑ Bonnefond S, Catroux M, Melenotte C, Karkowski L, Rolland L, Trouillier S, Raffray L (2016). “Clinical features of actinomycosis: A retrospective, multicenter study of 28 cases of miscellaneous presentations”. Medicine (Baltimore). 95 (24): e3923. doi:10.1097/MD.0000000000003923. PMC 4998488. PMID 27311002.
- ↑ Sung HY, Lee IS, Kim SI, Jung SE, Kim SW, Kim SY, Chung MK, Kim WC, Oh ST, Kang WK (2011). “Clinical features of abdominal actinomycosis: a 15-year experience of a single institute”. J. Korean Med. Sci. 26 (7): 932–7. doi:10.3346/jkms.2011.26.7.932. PMC 3124725. PMID 21738348.
- ↑ Choi MM, Baek JH, Beak JH, Lee JN, Park S, Lee WS (2009). “Clinical features of abdominopelvic actinomycosis: report of twenty cases and literature review”. Yonsei Med. J. 50 (4): 555–9. doi:10.3349/ymj.2009.50.4.555. PMC 2730619. PMID 19718405.
- ↑ Smego RA (1987). “Actinomycosis of the central nervous system”. Rev Infect Dis. 9 (5): 855–65. PMID 3317731.
- ↑ Meethal AC, Pattamparambath M, Balan A, Kumar NR, Sathyabhama S (2016). “Actinomycotic Osteomyelitis of the Maxilla – A Delusive Presentation”. J Clin Diagn Res. 10 (7): ZJ01–3. doi:10.7860/JCDR/2016/19171.8086. PMC 5020198. PMID 27630971.
- ↑ Shikino K, Ikusaka M, Takada T (2015). “Cervicofacial actinomycosis”. J Gen Intern Med. 30 (2): 263. doi:10.1007/s11606-014-3001-z. PMC 4314475. PMID 25280832.
- ↑ Acevedo F, Baudrand R, Letelier LM, Gaete P (2008). “Actinomycosis: a great pretender. Case reports of unusual presentations and a review of the literature”. Int. J. Infect. Dis. 12 (4): 358–62. doi:10.1016/j.ijid.2007.10.006. PMID 18164641.
- ↑ Mani RK, Mishra V, Singh PK, Pradhan D (2017). “Pulmonary actinomycosis: a clinical surprise!”. BMJ Case Rep. 2017. doi:10.1136/bcr-2016-218959. PMID 28130291.
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Historical Perspective
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Yamuna Kondapally, M.B.B.S[2]
Overview
Actinomycosis was first discovered in 1877 in cattle by pathologist Otto Bollinger. Later in the year, James Israel discovered it in humans and classified it under fungal origin. In 1939, Bergey classified it into bacteria.
Historical Perspective
- In 1877, pathologist Otto Bollinger discovered for the first time, presence of Actinomyces bovis in cattle
- In 1877, James Israel discovered Actinomyces Israelii in humans.
- In 1890, Eugene Bostroem isolated the causative organism from a culture of grasses, grain, and soil.
- In 1939, Bergey’s Manual of Systematic Bacteriology classified the organism as bacterial.[1]
References
- ↑ Sullivan DC, Chapman SW (2010). “Bacteria that masquerade as fungi: actinomycosis/nocardia”. Proc Am Thorac Soc. 7 (3): 216–21. doi:10.1513/pats.200907-077AL. PMID 20463251.
Classification
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Yamuna Kondapally, M.B.B.S[2]
Overview
Actinomycosis is bacterial infection most commonly involving oro-facial tissues. It can be classified based on the anatomical site involved.
Classification
Actinomycosiscan be classified based on the anatomical site involved into[1]
- Orocervicofacial actinomycosis
- Thoracic actinomycosis
- Abdominopelvic actinomycosis
- Central nervous system actinomycosis
- Musculoskeletal actinomycosis
- Disseminated actinomycosis
References
- ↑ Valour F, Sénéchal A, Dupieux C, Karsenty J, Lustig S, Breton P, Gleizal A, Boussel L, Laurent F, Braun E, Chidiac C, Ader F, Ferry T (2014). “Actinomycosis: etiology, clinical features, diagnosis, treatment, and management”. Infect Drug Resist. 7: 183–97. doi:10.2147/IDR.S39601. PMC 4094581. PMID 25045274.
Pathophysiology
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aditya Ganti M.B.B.S. [2]
Overview
Actinomycosis is a chronic pyogenic bacterial infection caused by actinomyces species. Infection most frequently follows dental work, trauma, surgery, or other medical conditions. When there is break in the mucosa, anywhere from the mouth to the rectum they reach tissues and cause damage. Incubation period of actinomycosis varies from one to four weeks. But occasionally, it may be as long as several months. Actinomycosis elicits both humoral and cell-mediated immune responses
Pathophysiology
- Actinomycosis is caused by the bacteria Actinomyces. The pathophysiology of actinomycosis can be described in the following steps. [1][2][3][4][5][6]
Transmission
- Actinomyces are part of the natural flora of human body, resides in the oral cavity, lower gastrointestinal tract and urogenital tract.
- They are nonvirulent under normal conditions
- When there is a breach in normal mucosal architecture, anywhere from the mouth to the rectum they enter tissues and cause damage.
| Types | Site of Infection | Source of infection |
|---|---|---|
| Cervicofacial actinomycosis |
| |
| Thoracic |
| |
| Abdominal actinomycosis | Abdomen |
|
| Pelvic
actinomycosis |
Pelvis | |
| Central nervous system | CNS |
Incubation
Incubation period of actinomycosis varies from one to four weeks.
Dissemination
Following transmission, lesions spread by direct extension.
Seeding
- Once the endogenous bacteria are introduced into the tissues, they multiply due to low oxygen tension.
- It leads to the formation of hard yellow hard granules (sulfur granules).
- These granules represent solidified bacterial filaments with surrounding tissue exudates.
- These triggers an inflammatory reaction.
- Inflammatory mediators along with various bacterial toxins and proteolytic enzymes from the neutrophils are released leading to abscess formation.
- A fibrous wall develops around the abscess.
- Extension of the abscess to skin leads to the formation of sinus tracts and pus drains out through these sinuses.
Immune response
Actinomycosis elicits both humoral and cell-mediated immune responses
Genetics
There is no known genetic association to actinomycosis
Gross Pathology
On gross pathology, the following features can be noticed:
- Single or multiple abscesses
- Indurated masses with hard fibrous walls and soft central loculations containing white or yellow pus.
- Granules are seen grossly.
- Sinus tracts extended from abscesses to the skin surface or into organs; vertebral bone, and retroperitoneal tissue.
- Pleural, pericardial, or serosal thickening if the infection involves lung, heart, and wall of the bowel.
Microscopic pathology
Microscopic findings include
- Liquefaction type of necrosis in the center of abscess with a surrounding outer layer of granulation tissue along with lymphocytes and neutrophils.
- Gram-positive organism with branching filaments like structures appear as colonies.

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References
- ↑ Volante M, Contucci AM, Fantoni M, Ricci R, Galli J (2005). “Cervicofacial actinomycosis: still a difficult differential diagnosis”. Acta Otorhinolaryngol Ital. 25 (2): 116–9. PMC 2639881. PMID 16116835.
- ↑ Sharkawy AA (2007). “Cervicofacial actinomycosis and mandibular osteomyelitis”. Infect. Dis. Clin. North Am. 21 (2): 543–56, viii. doi:10.1016/j.idc.2007.03.007. PMID 17561082.
- ↑ Peipert, Jeffrey F. (2004). “Actinomyces: Normal Flora or Pathogen?”. Obstetrics & Gynecology. 104 (Supplement): 1132–1133. doi:10.1097/01.AOG.0000145267.59208.e7. ISSN 0029-7844.
- ↑ Higashi Y, Nakamura S, Ashizawa N, Oshima K, Tanaka A, Miyazaki T, Izumikawa K, Yanagihara K, Yamamoto Y, Miyazaki Y, Mukae H, Kohno S (2017). “Pulmonary Actinomycosis Mimicking Pulmonary Aspergilloma and a Brief Review of the Literature”. Intern. Med. 56 (4): 449–453. doi:10.2169/internalmedicine.56.7620. PMID 28202870.
- ↑ Schaal KP, Lee HJ (1992). “Actinomycete infections in humans–a review”. Gene. 115 (1–2): 201–11. PMID 1612438.
- ↑ Brown, James R. (1973). “Human actinomycosisA study of 181 subjects”. Human Pathology. 4 (3): 319–330. doi:10.1016/S0046-8177(73)80097-8. ISSN 0046-8177.
- ↑ Smego RA (1987). “Actinomycosis of the central nervous system”. Rev Infect Dis. 9 (5): 855–65. PMID 3317731.
Causes
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Actinomyces israelii is a species of Gram-positive, rod-shaped bacteria within the Actinomyces. Known to live commensally on and within humans, A. israelii is an opportunistic pathogen and a cause of actinomycosis. Many physiologically diverse strains of the species are known to exist, though all are strict anaerobes.[1]
Pathogenesis
Actinomycosis is most frequently caused by A. israelii. It is a normal colonizer of the vagina,[2] colon, and mouth. Infection is established first by a breach of the mucosal barrier during various procedures (dental, gastrointestinal), aspiration, or pathologies such as diverticulitis. The chronic phase of this disease is also known the “classic phase” because the acute, early phase is often missed by health care providers. This is characterized by slow, contiguous growth that ignores tissue planes and forms a sinus tract that can spontaneously heal and recur, leading to a densely fibrotic lesion. This lesion is often characterized as “wooden”. Sulfur granules form in a central purulence surrounded by neutrophils. This conglomeration of organisms is virtually diagnostic of A. israelii.
References
- ↑ Levinson, W. Review of Medical Microbiology and Immunology. 2010:McGraw Hill.
- ↑ Hoffman, Barbara (2012). Williams gynecology, 2nd edition. New York: McGraw-Hill Medical. p. 65. ISBN 0071716726.
Differentiating Actinomycosis from other Diseases

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aditya Ganti M.B.B.S. [2]
Overview
Based on the organ system involved and duration of symptoms, differential diagnosis of actinomycosis consists of blastomycosis, brain abscess, colon cancer, crohn disease, diverticulitis, liver abscess, lung abscess, lymphoma, nocardiosis, pelvic inflammatory disease, pneumonia, tuberculosis and uterine cancer.
Differential Diagnosis
- Actinomycosis is a chronic pyogenic bacterial infection caused by Actinomycesspecies and most commonly involves orocervicofacial region
- It rarely infects other organ systems. If involved it has a wide variety of presentation.
- Most common symptoms of actinomycosis includes abscess with draining sinus tracts.
- Other symptoms are mostly non-specific for actinomycosis.
- Based on the organ system involved and duration of symptoms it should be differentiated from other conditions:[1][2][3][4][5][6][7][8][9] [10]
| System involved | Disease | Differentiating signs/symptoms | Differentiating tests |
|---|---|---|---|
| Abdomen | Abdominal Abscess | Features of sepsis and signs of an acute abdomen are generally prominent | Histology and culture for actinomycetes are negative.
Blood cultures positive for the causative organism. |
| Appendicitis | Rapid onset of symptoms
Positive for signs of appendicitis |
Ultrasound shows inflammation of appendix
Negative blood culture | |
| Colon cancer | Systemic findings like weight loss, night sweats present
Blood loss in stools |
Colonoscopy identifies the lesions, histopathology confirms the presence of the malignant cells. | |
| Whipple disease | An acute GI illness, with fever, diarrhea, and weight loss
Malabsorption such as steatorrhea. Abdominal lymphadenopathy and abdominal pain. Joint problems |
Anti-Tropheryma whipplei-positive macrophage (Tropheryma whipplei).
PCR testing of duodenal biopsies positive for T whipplei | |
| Inflammatory bowel disease | Dysentery | Colonoscopy identifies the ulcerative lesions | |
| Pulmonary | Nocardiosis | Immunocompromised host
Predominant pulmonary |
Modified acid-fast staining of biopsy tissue or other samples allows distinction between Nocardia and Actinomyces |
| Blastomycosis | Self-limited
Cutaneous manifestations along with lung involvement. Endemic to Mississippi and Ohio river valley |
Sputum smear and culture using KOH preparations or specific stains can confirm diagnosis | |
| Lung abscess | Risk of aspiration
Cough with foul smelling sputum |
Polymicrobial infection | |
| Pulmonary tuberculosis | Cough >2 weeks | Acid fast bacilli positive on sputum examination
Tuberculin skin testing positive. | |
| Uro-genital system | Ovarian/Oviductal tumor | Systemic findings like weight loss ,night sweats present
No leukorrhea |
Histopathology shows malignancy. |
| Pelvic inflammatory disease | History of recent sexual contact or a sexually transmitted infection in the partner,
Past history of PID. |
Laparoscopy with biopsy sampling followed by histology. |
- The clinical manifestations of actinomycosis and nocardiosis are similar. The following table helps in differentiating actinomycosis from nocardiosis.[11][12]
- Differentiation of actinomycosis from nocardiosis is very important in selection of appropriate antimicrobial therapy.[13][14]
| Actinomycosis | Nocardiosis |
|---|---|
| Gram positive anaerobic species | Gram positive aerobe |
| Decreasing incidence | Increasing incidence |
| Occurs primarily in immunocompetent host | Occurs primarily in immunocompromised host |
| Predominant cervicofacial | Predominant pulmonary |
| Chest wall involvement and bony erosions are common | Chest wall involvement is uncommon |
| Granuloma formation and intense fibrosis are common. Form characteristic sulfur granules | Granuloma formation and fibrosis are uncommon |
| Spread by direct invasion | Metastatic spread is common (especially to brain) |
| Diagnosis is made through cytologic or histologic examination | Diagnosis is made through bronchoalveolar lavage (BAL). |
| Treatment: Penicillin
Treatment with antibiotics alone |
Treatment: Sulfonamides
Often need surgical drainage |
References
- ↑ Yiğiter M, Kiyici H, Arda IS, Hiçsönmez A (2007). “Actinomycosis: a differential diagnosis for [[appendicitis]]. A case report and review of the literature”. J Pediatr Surg. 42 (6): E23–6. doi:10.1016/j.jpedsurg.2007.03.057. PMID 17560191. URL–wikilink conflict (help)
- ↑ Hasper D, Schefold JC, Baumgart DC (2009). “Management of severe abdominal infections”. Recent Pat Antiinfect Drug Discov. 4 (1): 57–65. PMID 19149697.
- ↑ Lederman ER, Crum NF (2004). “A case series and focused review of nocardiosis: clinical and microbiologic aspects”. Medicine (Baltimore). 83 (5): 300–13. doi:10.1097/01.md.0000141100.30871.39. PMID 15342974.
- ↑ Hoffman, Barbara (2012). Williams gynecology. New York: McGraw-Hill Medical. ISBN 9780071716727.
- ↑ Humes, D J (2006). “Acute appendicitis”. BMJ. 333 (7567): 530–534. doi:10.1136/bmj.38940.664363.AE. ISSN 0959-8138.
- ↑ Saccente M, Woods GL (2010). “Clinical and laboratory update on blastomycosis”. Clin. Microbiol. Rev. 23 (2): 367–81. doi:10.1128/CMR.00056-09. PMC 2863359. PMID 20375357.
- ↑ Kim, Eun Ran (2014). “Colorectal cancer in inflammatory bowel disease: The risk, pathogenesis, prevention and diagnosis”. World Journal of Gastroenterology. 20 (29): 9872. doi:10.3748/wjg.v20.i29.9872. ISSN 1007-9327.
- ↑ Hanauer, Stephen B. (1996). “Inflammatory bowel disease”. New England Journal of Medicine. 334 (13): 841–848. PMID 8596552. Retrieved 2006-11-10.
- ↑ Kuhajda I, Zarogoulidis K, Tsirgogianni K, Tsavlis D, Kioumis I, Kosmidis C, Tsakiridis K, Mpakas A, Zarogoulidis P, Zissimopoulos A, Baloukas D, Kuhajda D (2015). “Lung abscess-etiology, diagnostic and treatment options”. Ann Transl Med. 3 (13): 183. doi:10.3978/j.issn.2305-5839.2015.07.08. PMC 4543327. PMID 26366400.
- ↑ Soper DE (2010). “Pelvic inflammatory disease”. Obstet Gynecol. 116 (2 Pt 1): 419–28. doi:10.1097/AOG.0b013e3181e92c54. PMID 20664404.
- ↑ Sullivan DC, Chapman SW (2010). “Bacteria that masquerade as fungi: actinomycosis/nocardia”. Proc Am Thorac Soc. 7 (3): 216–21. doi:10.1513/pats.200907-077AL. PMID 20463251.
- ↑ Warren NG (1996). “Actinomycosis, nocardiosis, and actinomycetoma”. Dermatol Clin. 14 (1): 85–95. PMID 8821161.
- ↑ Smego RA (1987). “Actinomycosis of the central nervous system”. Rev Infect Dis. 9 (5): 855–65. PMID 3317731.
- ↑ Bassiri-Jahromi S, Doostkam A (2011). “Actinomyces and nocardia infections in chronic granulomatous disease”. J Glob Infect Dis. 3 (4): 348–52. doi:10.4103/0974-777X.91056. PMC 3249989. PMID 22223997.
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Epidemiology and Demographics
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aditya Ganti M.B.B.S. [2]
Overview
In 1970, the annual incidence of actinomycosis was estimated to be 1 per 300,000. Since then it’s incidence has been declined due to the widespread use of antibiotics following dental surgeries. Actinomycosis is commonly found between 4th to 6th decade of life and very rare in infants and children. Males are more commonly affected by actinomycosis than females.
Epidemiology and Demographics
Incidence
- Actinomycosis is a rare disease, and not all cases gets reported.
- Estimating its annual incidence is difficult because, most of the infections are are not diagnosed and are treated empirically[1][2]
- Widespread use of antibiotics following dental surgeries also lead to its decreased incidence.
- In 1970, its annual incidence was 1 per 300,000.
Age
Actinomycosis is commonly found between 4th to 6th decade of life and very rare in infants and children
Gender
Males are more commonly affected by actinomycosis than females.
References
- ↑ Bonnefond S, Catroux M, Melenotte C, Karkowski L, Rolland L, Trouillier S, Raffray L (2016). “Clinical features of actinomycosis: A retrospective, multicenter study of 28 cases of miscellaneous presentations”. Medicine (Baltimore). 95 (24): e3923. doi:10.1097/MD.0000000000003923. PMC 4998488. PMID 27311002.
- ↑ Vielkind P, Jentsch H, Eschrich K, Rodloff AC, Stingu CS (2015). “Prevalence of Actinomyces spp. in patients with chronic periodontitis”. Int. J. Med. Microbiol. 305 (7): 682–8. doi:10.1016/j.ijmm.2015.08.018. PMID 26324012.
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Risk Factors
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Aditya Ganti M.B.B.S. [2]
Overview
Common risk factors in the development of actinomycosis include dental abscess, oral surgery, and facial trauma.
Risk Factors
Risk factors of actinomycosis include:[1][2]
| Types | Risk Factors |
|---|---|
| Cervicofacial actinomycosis |
|
| Thoracic actinomycosis | |
| Abdominal actinomycosis |
|
| Pelvic actinomycosis |
|
| CNS actinomycosis |
References
- ↑ Knapman P (1985). “The long arm of the coroner”. Med Leg J. 53 ( Pt 4): 206–21. doi:10.1177/002581728505300406. PMID 4094581.
- ↑ Smego RA (1987). “Actinomycosis of the central nervous system”. Rev Infect Dis. 9 (5): 855–65. PMID 3317731.
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Screening
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Aditya Ganti M.B.B.S. [2]
Overview
There are no screening recommendations for actinomycosis.
References
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Natural History, Complications and Prognosis
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aditya Ganti M.B.B.S. [2]
Overview
Once in the tissue, actinomyces multiply and forms an abscess, producing a hard, red to reddish-purple lump, most commonly on the jaw. Eventually, the abscess ruptures through the skin surface producing a draining sinus tract. If left untreated, patients with actinomycosis may progress to develop multiple abscesses which can heal and reappear. The prognosis is excellent with prompt and effective antimicrobial treatment. Complications that can develop as a result of actinomycosis are osteomyelitis, endocarditis, pericarditis and meningitis.
Natural History
- Once in the tissue, actinomyces multiply and forms an abscess, producing a hard, red to reddish-purple lump, often on the jaw.
- Eventually, the abscess ruptures through the skin surface to produce a draining sinus tract and are completely treatable.
- If left untreated, patients with actinomycosis may progress to develop focal organ involvement with mass-like features and multiple abscesses which can heal and reform.[1][2][3][4][5][6]
Prognosis
- The prognosis is excellent with prompt and effective antimicrobial treatment in patients with uncomplicated actinomycosis that does not affect the CNS.
- The factors that define the outcomes of the disease include:
- Site of infection
- The time to diagnose
- The time to the start of appropriate treatment
- Mortality range from 0% to 28% highest being in CNS.
Complications
Complications that can develop as a result of actinomycosis are [7]
- Extension of disease can result in osteomyelitis of the mandible, ribs, or vertebrae.
- Endocarditis
- Pericarditis
- Brain abscess
- Meningitis
References
- ↑ Volante M, Contucci AM, Fantoni M, Ricci R, Galli J (2005). “Cervicofacial actinomycosis: still a difficult differential diagnosis”. Acta Otorhinolaryngol Ital. 25 (2): 116–9. PMC 2639881. PMID 16116835.
- ↑ Sharkawy AA (2007). “Cervicofacial actinomycosis and mandibular osteomyelitis”. Infect. Dis. Clin. North Am. 21 (2): 543–56, viii. doi:10.1016/j.idc.2007.03.007. PMID 17561082.
- ↑ Peipert, Jeffrey F. (2004). “Actinomyces: Normal Flora or Pathogen?”. Obstetrics & Gynecology. 104 (Supplement): 1132–1133. doi:10.1097/01.AOG.0000145267.59208.e7. ISSN 0029-7844.
- ↑ Higashi Y, Nakamura S, Ashizawa N, Oshima K, Tanaka A, Miyazaki T, Izumikawa K, Yanagihara K, Yamamoto Y, Miyazaki Y, Mukae H, Kohno S (2017). “Pulmonary Actinomycosis Mimicking Pulmonary Aspergilloma and a Brief Review of the Literature”. Intern. Med. 56 (4): 449–453. doi:10.2169/internalmedicine.56.7620. PMID 28202870.
- ↑ Schaal KP, Lee HJ (1992). “Actinomycete infections in humans–a review”. Gene. 115 (1–2): 201–11. PMID 1612438.
- ↑ Brown, James R. (1973). “Human actinomycosisA study of 181 subjects”. Human Pathology. 4 (3): 319–330. doi:10.1016/S0046-8177(73)80097-8. ISSN 0046-8177.
- ↑ Agrawal P, Vaiphei K (2014). “Renal actinomycosis”. BMJ Case Rep. 2014. doi:10.1136/bcr-2014-205892. PMC 4244330. PMID 25406215.
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Acknowledgements
Acknowledgements
The content on this page was first contributed by: Dr. Steve Wiviott
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