Actinomycosis 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]

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	Neck Jaw Mouth	Dental problems like tooth decay
Thoracic actinomycosis	Lungs Pleura Chest wall Mediastinum	Inhalation of droplets of contaminated fluid Aspiration of oropharyngeal secretions or gastric contents Direct extension of cervicofacial infection into the mediastinum Transdiaphragmatic or retroperitoneal spread from the abdomen Hematogenous spread
Abdominal actinomycosis	Abdomen	Secondary to abdominal infections like appendicitis Accidental swallowing of a foreign body such as chicken bone containing the actinomycetes bacteria Penetrating trauma Perforation of the gut (e.g., the colon or appendix) Surgical manipulation of GI tract
Pelvic actinomycosis	Pelvis	Occurs most commonly in woman as the bacteria enters into the pelvis Long-term use of IUD type of contraceptive
Central nervous system actinomycosis	CNS	Secondary to hematogenous spread from primary infection in the lung, abdomen, or pelvis Direct extension from paranasal sinuses, ears, and cervicofacial regions^[7]

Incubation period of actinomycosis varies from one to four weeks.

Following transmission, lesions spread by direct extension.

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.

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.

Overview