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Actinomycosis is a rare subacute or chronic bacterial infection that causes both suppurative and granulomatous inflammation. Characteristics include localised swelling with suppuration, abscess formation, fibrosis and sinus drainage of pus containing 'sulfur granules'.

Actinomycetes are normal colonising organisms of the oral cavity and may also be present in the lower gastrointestinal and genitourinary tracts. They should be considered facultatively pathogenic commensals, requiring a break in the mucous membranes or devitalised tissue to invade deeper body structures and cause illness.

Actinomycosis is almost invariably a synergistically mixed infection of several species of actinomyces and other bacteria - some would consider the plural actinomycoses more correct because of this poly-aetiology. Actinomyces israelii and A. gerencseriae are the most commonly encountered organisms in the human forms of the disease. Less common species include A. naeslundii, A. odontolyticus, A. viscosus, A. meyeri, A. turicensis and A. radingae[1].

Infections tend to develop in tissue adjacent to mucous membranes; oral and cervicofacial infections are most common but any body site can be infected and, rarely, disseminated spread can occur.

Actinomycosis is a great 'mimic'; symptoms and signs may initially be thought to be due to other diseases, particularly malignancy[2]. Failure to consider the diagnosis can lead to unnecessary surgery and delay in adequate treatment.

  • Actinomycosis is rare.
  • The incidence of all forms of actinomycosis is thought to have declined in recent years, especially in developed countries, as a result of better oral hygiene and susceptibility to a broad range of antibiotics.

Risk factors[1]

  • Age 20-60 years.
  • Male sex (except for pelvic actinomycosis, which mainly affects women).
  • Diabetes.
  • Immunosuppression: steroids, bisphosphonates, leukaemia treated with chemotherapy, HIV, lung and renal transplant receipts, alcoholism, local tissue damage (caused by trauma, recent surgery or irradiation).
  • Poor oral hygiene with dental decay.
  • Previous abdominal surgery.

The presentation depends on the part of the body infected:


  • The most common form and accounts for about 50% of all reported cases.
  • Usually follows dental manipulation or trauma to the mouth but can occur spontaneously in patients with poor dental hygiene.
  • Common presenting features include fever and chronic painless or painful soft tissue swelling around the mandible.
  • Lesions may develop a firm woody consistency that often leads to a misdiagnosis of malignancy.
  • Regional lymphadenopathy is typically absent until later stages.
  • Infection may extend into local structures such as bone (periostitis and osteomyelitis) and muscle.


  • Accounts for 15-20% of cases.
  • Infection usually results from aspiration of oropharyngeal secretions. May also occur after oesophageal perforation, local spread from cervicofacial or abdominal infection, or from haematogenous spread.
  • A higher incidence has been reported in patients with underlying lung disorders.
  • Initially the clinical picture may be of pneumonia with a low-grade fever, cough, shortness of breath, and chest pain. There is usually a longer history of illness and associated weight loss and haemoptysis.
  • Complications include the spread of infection to soft tissues of the chest wall, pleural effusion, mediastinal invasion and rib destruction. Mediastinal disease can progress into the heart to cause pericarditis, and less often myocarditis and endocarditis.


  • Accounts for about 20% of cases.
  • Acute appendicitis, especially with perforation, accounts for most cases and may present with a mass in the right iliac fossa[3].
  • Other predisposing factors include gastrointestinal perforation, previous surgery, neoplasia and foreign bodies in the gastrointestinal tract or genitourinary tract.
  • May present with nonspecific symptoms such as fever, weight loss and abdominal pain.
  • There may not always be a palpable mass. Fewer than 10% of cases are diagnosed pre-operatively.
  • Infection can spread directly into neighbouring tissues, and sinus tracts may form into the abdominal wall or the perianal region.
  • Abdominal disease can spread directly into the pelvis but pelvic actinomycosis is predominantly associated with intrauterine contraceptive devices (IUCDs). It usually presents with a history of prolonged use (>2 years) and symptoms of fever, vaginal discharge, pelvic or abdominal pain, and weight loss.
  • Rare sites of actinomycosis include the central nervous system (CNS), bones, muscle tissue and any prosthetic joints.


  • This is rare.
  • It usually occurs as a result of haematogenous spread or direct extension of orocervicofacial infection. CNS disease may include brain abscess, meningitis, meningoencephalitis, actinomycoma, subdural empyema and epidural abscess.
  • Non-meningitic infection usually presents as a space-occupying lesion with symptoms of headache and focal neurological signs.


  • This is rare.
  • It is usually caused by spread from adjacent soft tissue but can also be from local trauma or haematogenous spread.
  • The facial bones, especially the mandible, are the most common sites of bone disease.


  • All species of actinomyces are capable of haematogenous spread but disseminated actinomycosis is very rare since the development of antibiotics.

This depends upon the site but includes:

  • Blood tests: nonspecific but there may be evidence of anaemia, mild leukocytosis, raised ESR and CRP and raised alkaline phosphatase (in hepatic actinomycosis).
  • CT and MRI scans usually show nonspecific features of an abscess but do provide accurate anatomical localisation, which can aid tissue sampling.
  • Histopathology: Gram-positive filamentous organisms and 'sulfur granules' on histological examination are strongly supportive of a diagnosis of actinomycosis. A species-specific fluorescent antibody allows rapid identification by direct staining, even after fixation in formalin.
  • Microbiology: direct isolation of the organism from a clinical specimen or from 'sulfur granules' is necessary for a definitive diagnosis. However, the failure rate of isolation is high.
  • Serological assays have been developed but sensitivity and specificity need to be improved before they become clinically useful.
  • Molecular genetic methods, such as polymerase chain reaction, rRNA sequencing, fluorescence in situ hybridisation and mass spectrometry, are available for more rapid and accurate identification in reference or research laboratories.


  • Patients with all forms of actinomycosis have historically been treated with high doses of intravenous penicillin G over 2-6 weeks, followed by oral penicillin V for 6-12 months. The risk of actinomyces developing penicillin resistance is low.
  • Actinomyces are susceptible to a wide range of antimicrobial agents, such as beta-lactams (including benzylpenicillin, amoxicillin, ceftriaxone, meropenem and piperacillin-tazobactam), doxycycline, clindamycin, erythromycin and clarithromycin.
  • The initial phase of treatment should cover other bacteria found at the site of infection. A first-line regimen might consist of a beta-lactam and a beta-lactamase inhibitor such as clavulanate or tazobactam, which offers additional cover against potential beta-lactamase producers such as Staphylococcus aureus and Gram-negative anaerobes.
  • In abdominal actinomycosis, a possible treatment of choice is a combination of amoxicillin and clavulanic acid with metronidazole (or clindamycin) for strict anaerobes plus an aminoglycoside for resistant Enterobacteriaceae.
  • The duration of antibiotic treatment will vary. The traditional recommendation of 6-12 months may not be needed for all patients. Shorter courses of treatment may be sufficient, with or without additional surgical drainage.


  • Surgical resection of infected tissue may also be necessary in some cases, especially if extensive necrotic tissue, sinus tracts, or fistulas are present.
  • Surgery may also be needed if malignancy cannot be excluded or if large abscesses or empyemas cannot be drained by percutaneous aspiration.
  • Surgery may be a valid option for patients who do not respond to medical treatment.

A cervical smear may show actinomycete-like organisms (ALOs), especially if an IUCD is in situ; however, without clinical evidence of PID they are not significant[5, 6]. The finding of actinomyces does not require treatment or removal of the IUCD unless there are clinical features of disease[7].

Actinomycosis is increasingly being recognised as a major factor and poor prognostic indicator in infected osteoradionecrosis and bisphosphonate-associated osteonecrosis of the jaws[9].

  • Reports of mortality range from 0% to 28% depending on the site of infection, the time to diagnosis and the time to the start of appropriate treatment.
  • The highest mortality occurs in CNS disease.

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Further reading and references

  1. Wong VK, Turmezei TD, Weston VC; Actinomycosis. BMJ. 2011 Oct 11343:d6099. doi: 10.1136/bmj.d6099.

  2. Acevedo F, Baudrand R, Letelier LM, et al; Actinomycosis: a great pretender. Case reports of unusual presentations and a review of the literature. Int J Infect Dis. 2008 Jul12(4):358-62. Epub 2008 Mar 4.

  3. Jarry J, Shekher M, Imperato M, et al; Appendicitis: When there is more than meets the eye. Clin Res Hepatol Gastroenterol. 2011 Nov35(11):765-7. doi: 10.1016/j.clinre.2011.05.014. Epub 2011 Jul 16.

  4. Yigiter M, Kiyici H, Arda IS, et al; Actinomycosis: a differential diagnosis for appendicitis. A case report and review of the literature. J Pediatr Surg. 2007 Jun42(6):E23-6.

  5. Merki-Feld GS, Rosselli M, Imthurn B; Comparison of two procedures for routine IUD exchange in women with positive Pap smears for actinomyces-like organisms. Contraception. 2008 Mar77(3):177-80. doi: 10.1016/j.contraception.2007.11.007. Epub 2008 Jan 11.

  6. Westhoff C; IUDs and colonization or infection with Actinomyces. Contraception. 2007 Jun75(6 Suppl):S48-50. Epub 2007 Mar 23.

  7. Penney G, Brechin S, de Souza A, et al; FFPRHC Guidance (January 2004). The copper intrauterine device as long-term contraception. J Fam Plann Reprod Health Care. 2004 Jan30(1):29-41

  8. Kanellopoulou T, Alexopoulou A, Tanouli MI, et al; Primary hepatic actinomycosis. Am J Med Sci. 2010 Apr339(4):362-5. doi: 10.1097/MAJ.0b013e3181cbf47c.

  9. Hall V; Actinomyces--gathering evidence of human colonization and infection. Anaerobe. 2008 Feb14(1):1-7. Epub 2007 Dec 5.