eMedicine Specialties > Infectious Diseases > Bacterial Infections

Actinomycosis

Jason F Okulicz, MD, Assistant Professor of Medicine, Uniformed Services University of the Health Sciences; Staff, Infectious Disease Service, Brooke Army Medical Center
Hari Polenakovik, MD, Consultant Physician in Infectious Diseases and General Medicine, Department of Medicine, Western Health, Australia; Sylvia Polenakovik, MD, Clinical Instructor, Internist, Department of Internal Medicine, Wayne Hospital, Wright State University

Updated: Feb 24, 2009

Introduction

Background

Actinomycosis is a subacute-to-chronic bacterial infection caused by filamentous, gram-positive, non–acid-fast, anaerobic-to-microaerophilic bacteria. It is characterized by contiguous spread, suppurative and granulomatous inflammation, and formation of multiple abscesses and sinus tracts that may discharge sulfur granules. The most common clinical forms of actinomycosis are cervicofacial (ie, lumpy jaw), thoracic, and abdominal. In women, pelvic actinomycosis is possible.

For additional information on actinomycosis, see the articles Actinomycosis in eMedicine’s Dermatology volume, Actinomycosis in eMedicine’s Pediatrics: General Medicine volume, and Actinomycosis in eMedicine’s Ophthalmology volume.

Pathophysiology

Actinomycetes are prominent among the normal flora of the oral cavity but less prominent in the lower gastrointestinal tract and female genital tract. Because these microorganisms are not virulent, they require a break in the integrity of the mucous membranes and the presence of devitalized tissue to invade deeper body structures and to cause human illness.

Furthermore, actinomycosis is generally a polymicrobial infection, with isolates numbering as many as 5-10 bacterial species. Establishment of human infection may require the presence of such companion bacteria, which participate in the production of infection by elaborating a toxin or enzyme or by inhibiting host defenses. These companion bacteria appear to act as copathogens that enhance the relatively low invasiveness of actinomycetes. Specifically, they may be responsible for the early manifestations of actinomycosis and for treatment failures.

Once infection is established, the host mounts an intense inflammatory response (ie, suppurative, granulomatous), and fibrosis may then follow. Infection typically spreads contiguously, frequently ignoring tissue planes and invading surrounding tissues or organs. Ultimately, the infection produces draining sinus tracts. Hematogenous dissemination to distant organs may occur in any stage of actinomycosis, whereas lymphatic dissemination is unusual.

Cervicofacial actinomycosis

Cervicofacial actinomycosis is the most common type of the infection, comprising 50-70% of reported cases. This infection typically occurs following oral surgery or in patients with poor dental hygiene. Cervicofacial actinomycosis is characterized in the initial stages by soft-tissue swelling of the perimandibular area. Direct spread into the adjacent tissues occurs over time, along with development of fistulas (sinus tracts) that discharge purulent material containing granules with a yellow sulfurlike appearance (termed sulfur granules). Invasion of the cranium or the bloodstream may occur if the disease is left untreated.

Thoracic actinomycosis

Thoracic actinomycosis accounts for 15-20% of cases. Aspiration of oropharyngeal secretions containing actinomycetes is the usual mechanism of infection. Occasionally, thoracic actinomycosis results from the introduction of organisms via esophageal perforation, by direct spread from an actinomycotic process of the neck or abdomen, or via hematogenous spread from a distant lesion. Thoracic actinomycosis commonly presents as a pulmonary infiltrate or mass, which, if left untreated, can spread to involve the pleura, pericardium, and chest wall, ultimately leading to the formation of sinuses that discharge sulfur granules.

Actinomycosis of the abdomen and pelvis

Actinomycosis of the abdomen and pelvis accounts for 10-20% of reported cases. Typically, these patients have a history of recent or remote bowel surgery (eg, perforated acute appendicitis, perforated colonic diverticulitis following trauma to the abdomen) or ingestion of foreign bodies (eg, chicken or fish bones), during which actinomycetes are introduced into the deep tissues. The ileocecal region is involved most frequently, and the disease typically presents as a slowly growing tumor. Diagnosis is usually established postoperatively, following exploratory laparotomy for a suspected malignancy. Involvement of any abdominal organ, including the abdominal wall, can occur by direct spread, with eventual formation of draining sinuses. Pelvic actinomycosis most commonly ascends from the uterus in association with intrauterine contraceptive devices (IUCDs). In such cases, an IUCD has been in place for an average of 8 years.

Frequency

United States

Actinomycosis is rare. During the 1970s, the reported annual incidence of actinomycosis in the Cleveland area was 1 case per 300,000 persons. Improved dental hygiene and widespread use of antibiotics for various infections have probably contributed to the declining incidence of this disease.

International

Actinomycosis occurs worldwide, with likely higher prevalence rates in areas with low socioeconomic status and poor dental hygiene.

Mortality/Morbidity

The availability of antibiotics has greatly improved the prognosis of all forms of actinomycosis. At present, cure rates are high, and neither deformity nor death is common.

Race

Actinomycosis has no racial predilection.

Sex

For unknown reasons, actinomycosis is more common in men than in women (male-to-female ratio, 3:1), with the exception of pelvic actinomycosis.

Age

Actinomycosis can affect people of all ages, but most cases are reported in young to middle-aged adults (aged 20-50 y).

Clinical

History

  • Cervicofacial actinomycosis (ie, lumpy jaw)
    • History of dental manipulation or trauma to the mouth, poor oral hygiene, dental caries, or periodontal disease; may arise following local tissue damage caused by neoplasm or by osteonecrosis of the jaw or maxilla due to radiation treatment or bisphosphonate use1,2,3,4
    • Painless or occasionally painful soft-tissue swelling involving the submandibular or perimandibular region; over time, multiple sinuses drain pus containing sulfur granules; tendency to remit and recur
    • Reddish or bluish discoloration of the skin overlying the lesion
    • Chewing difficulties (ie, with involvement of mastication muscles)
  • Thoracic actinomycosis
    • History of aspiration (Risk factors include seizure disorder, alcoholism, and poor dental hygiene.)
    • Dry or productive cough, occasionally blood-streaked sputum, shortness of breath, chest pain
    • Fever, weight loss, fatigue, anorexia
  • Abdominal actinomycosis
    • History of abdominal surgery, perforated viscus, mesenteric vascular insufficiency, or ingestion of foreign bodies (eg, fish or chicken bones)
    • Nonspecific symptoms; the most common symptoms are as follows:
      • Low-grade fever
      • Weight loss
      • Fatigue
      • Change in bowel habits
      • Vague abdominal discomfort
      • Nausea
      • Vomiting
      • Sensation of a mass
  • Pelvic actinomycosis
    • History of IUCD
    • Lower abdominal discomfort, abnormal vaginal bleeding or discharge

Physical

  • Cervicofacial actinomycosis
    • Patients with cervicofacial actinomycosis present with nodular lesion(s), usually located at the angle of the jaw. These gradually increase in size and number (ie, multiple abscesses), and ultimately form sinuses that open onto the cheek or submandibular area. Sulfur granules may be seen in the exudate.
    • Nodules may be tender in the initial stages are typically nontender and woody hard in the later stages.
    • Lymphadenopathy is typically absent.
    • Trismus is present if the mastication muscles are involved.
    • Fever is variably present.
  • Thoracic actinomycosis
    • Fever, cachexia, abnormal breath sounds, cough (dry or productive of purulent sputum), hemoptysis
    • Sinus tracts with drainage from the chest wall (ie, pleurocutaneous fistula)
  • Abdominal actinomycosis
    • Scar(s) from antecedent abdominal surgery
    • Low-grade fever and cachexia (variably present)
    • Mass most often located in the right lower quadrant, less frequently in the left lower quadrant; mass typically firm-to-hard in consistency, nontender, often fixed to underlying tissue
    • Sinus tracts with drainage from either the abdominal wall (ie, peritoneocutaneous fistula) or the perianal region
  • Pelvic actinomycosis
    • Pelvic mass
    • Menometrorrhagia
    • Other manifestations, as in abdominal actinomycosis

Causes

Actinomycosis is caused by filamentous, gram-positive, non–acid-fast, non–spore-forming bacteria. They belong to the order of Actinomycetales, family Actinomycetaceae, genus Actinomyces. Members of the genera Propionibacterium, Actinobaculum, and Bifidobacterium may cause similar clinical syndromes. Actinomyces organisms grow slowly in anaerobic-to-microaerophilic conditions, forming colonies with a characteristic molar tooth appearance. The most common isolated species are Actinomyces israeli, Actinomyces gerencseriae, Actinomyces turicensis, Actinomyces radingae, and Actinomyces europaeus, followed by Actinomyces naeslundii, Actinomyces odontolyticus, Actinomyces viscosus, Actinomyces meyeri, and Propionibacterium propionicum.

In addition to these microorganisms, almost all actinomycotic lesions contain so-called companion bacteria. The most important of these bacteria is Actinobacillus actinomycetemcomitans, followed by Peptostreptococcus, Prevotella, Fusobacterium, Bacteroides, Staphylococcus, and Streptococcus species, and Enterobacteriaceae, depending on the location of actinomycotic lesions. These companion bacteria appear to magnify the low pathogenic potential of actinomycetes.

Differential Diagnoses

Abdominal Abscess
Lung Cancer, Oat Cell (Small Cell)
Adnexal Tumors
Lymphoma, Non-Hodgkin
Appendicitis
Malignant Neoplasms of the Small Intestine
Blastomycosis
Nocardiosis
Brain Abscess
Pelvic Inflammatory Disease
Colon Cancer, Adenocarcinoma
Pneumonia, Aspiration
Crohn Disease
Pneumonia, Bacterial
Diverticulitis
Pneumonia, Fungal
Liver Abscess
Tuberculosis
Lung Abscess
Uterine Cancer
Lung Cancer, Non-Small Cell

Other Problems to Be Considered

Abdominal mass
Epidural abscess

Workup

Laboratory Studies

  • CBC count: Anemia and mild leukocytosis are common.
  • Erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) levels are often elevated.
  • Chemistry results usually are normal, with the exception of a frequently elevated alkaline phosphatase level in hepatic actinomycosis.
  • Organism cultures
    • Because actinomycosis is difficult to diagnose based on the typical clinical features, direct identification and/or isolation of the infecting organism from a clinical specimen or from sulfur granules is necessary for definitive diagnosis in most cases.
    • Acceptable specimen material is obtained from draining sinuses, deep needle aspirate, or biopsy specimens; swabs, sputum, and urine specimens are unacceptable or inappropriate.
    • Prompt transport of the specimens to the microbiology laboratory is necessary for optimal isolation of actinomycetes, preferably in an anaerobic transport device.
    • A Gram-stained smear of the specimen may demonstrate the presence of beaded, branched, gram-positive filamentous rods, suggesting the diagnosis of actinomycosis.
    • Cultures should be placed immediately under anaerobic conditions and incubated for 48 hours or longer; the isolation and definitive identification of actinomycetes may require 2-3 weeks.
    • Nucleic acid probes and polymerase chain reaction (PCR) methods are being developed for more rapid and more accurate identification.
    • Antimicrobial susceptibility testing is not indicated in the management of actinomycosis, partly because of their predictable antibiogram.
  • The preliminary diagnosis of actinomycosis also can be made by examining sulfur granules. Granules should be crushed between 2 slides, stained with 1% methylene-blue solution, and examined microscopically for features characteristic of actinomycetes.
  • Serologic diagnosis: Current serologic tests have no role in diagnosing actinomycosis.
  • Papanicolaou test:
    • The relationship between a Papanicolaou test that is positive for actinomycetelike organisms and the eventual development of pelvic actinomycosis is unclear.
    • The prevalence of smears positive for Actinomyces organisms in women who use IUCDs is approximately 7%.5
    • Because of the lack of sensitivity and specificity and low positive predictive value, the prognostic significance of detecting Actinomyces organisms is minimal in the absence of concomitant symptoms.5

Imaging Studies

  • Chest radiography
    • A chest radiograph may reveal a poorly defined mass or pneumonitis or cavitary lesion, with or without pleural involvement. Hilar adenopathy is uncommon.
    • The presence of a masslike lesion that extends across fissures or pleura, invades into the adjacent chest wall or thoracic vertebrae, or causes local destruction of the ribs or sternum suggests thoracic actinomycosis.
  • CT scanning (irrespective of the anatomic area of involvement) usually reveals an infiltrative mass with focal areas of decreased attenuation that enhance with contrast. This infiltrative mass tends to invade surrounding tissues. Surrounding lymphadenopathy is uncommon.

Procedures

  • CT scan or ultrasound-guided fine-needle aspiration and/or biopsy have been used successfully to obtain clinical material for diagnosis of actinomycosis.
  • Surgery (eg, thoracotomy with open lung biopsy, exploratory laparotomy) may be required for diagnostic purposes.

Histologic Findings

Actinomycosis is characterized by mixed suppurative and granulomatous inflammatory reactions, connective-tissue proliferation, and the presence of sulfur granules. The sulfur granules are nearly pathognomonic for actinomycosis, although similar findings have been reported with infections caused by Nocardia brasiliensis, Streptomyces madurae, and Staphylococcus aureus presenting as botryomycosis. The granules are approximately 0.1-1 mm in diameter and may be seen with the naked eye as yellowish particles.

Microscopically, the granules manifest a cauliflowerlike shape at low magnification; at higher magnification (X100), when the particle has been pressed between slide and cover slip, a clump of filamentous actinomycete microcolonies surrounded by polymorphonuclear neutrophils (PMNs) can be observed. Gram stain renders these microcolonies visible as gram-positive, intertwined branching filaments, with radially arranged, peripheral hyphae. Coexisting with them are the companion bacteria, which are gram-positive and gram-negative cocci and rods. Image 1 and Image 2 are representative photomicrographs.

Treatment

Medical Care

In most cases of actinomycosis, antimicrobial therapy is the only treatment required, although surgery can be adjunctive in selected cases. Penicillin G is the drug of choice for treating infections caused by actinomycetes.

Surgical Care

Attempt to cure actinomycosis, including extensive disease, with aggressive antimicrobial therapy alone initially. Surgical therapy may include incision and drainage of abscesses, excision of sinus tracts and recalcitrant fibrotic lesions, decompression of closed-space infections, and interventions aimed at relieving obstruction (eg, when actinomycotic lesions compress the ureter).

Consultations

  • Interventional radiologist
  • Surgeon
  • Infectious diseases specialist

Diet

No specific dietary precautions are indicated in patients with actinomycosis.

Activity

Patients with actinomycosis may be active to the degree tolerated.

Medication

High-dose penicillin administered over a prolonged period (6 months to 1 year) is the cornerstone of therapy for actinomycosis. These recommendations were developed at a time when patients with actinomycosis typically presented late in the course of illness with large lesions, often receiving intermittent antibiotic therapy. In addition, modern imaging modalities were not available to monitor therapy. Success with shorter courses of therapy (<6 mo) has been reported, especially in cervicofacial actinomycosis.6 Ultimately, the treatment duration should be tailored to the individual patient based on clinical and radiographic response. Patients should be monitored more closely if shorter treatment durations are considered.

The risk of actinomycetes developing penicillin resistance appears to be minimal. Lack of a clinical response to penicillin usually indicates the presence of resistant companion bacteria, which may require modification of the antibiotic regimen (ie, addition of an agent that is active against these copathogens).

Antibiotics that possess no activity against Actinomyces species include metronidazole, aminoglycosides, aztreonam, co-trimoxazole (TMP-SMX), penicillinase-resistant penicillins (eg, methicillin, nafcillin, oxacillin, cloxacillin), and cephalexin. The data concerning the fluoroquinolones (ciprofloxacin, levofloxacin, moxifloxacin) are limited; however, treatment success has been cited in case reports.7,8

Antibiotics

Therapy must cover all likely pathogens in the context of this clinical setting.


Penicillin G (Pfizerpen, Bicillin)

DOC for treatment of actinomycosis. Interferes with synthesis of cell wall mucopeptide during active multiplication, resulting in bactericidal activity against susceptible microorganisms.

Dosing

Adult

12-24 million U/d IV by continuous infusion or in divided doses q4h for 1-2 wk, then switch to PO (penicillin VK) for 6-12 mo

Pediatric

200,000-400,000 U/kg/d IV by continuous infusion or in divided doses q4h for 1-2 wk, then switch to PO (penicillin VK) for 6-12 mo

Interactions

Probenecid can increase effects; coadministration of tetracyclines can decrease effects

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Caution in impaired renal function


Penicillin VK (Pen-Vee K, V-Cillin-K)

DOC for treatment of actinomycosis. Interferes with synthesis of cell wall mucopeptide during active multiplication, resulting in bactericidal activity against susceptible microorganisms.

Dosing

Adult

500 mg PO q6h for 6-12 mo

Pediatric

25-50 mg/kg/d PO in divided doses q6h for 6-12 mo

Interactions

Probenecid can increase effects; coadministration of tetracyclines can decrease effects

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Caution in impaired renal function


Doxycycline (Bio-Tab, Doryx, Vibramycin)

For nonpregnant patients with penicillin allergy. Inhibits protein synthesis and, thus, bacterial growth by binding to 30S and possibly 50S ribosomal subunits of susceptible bacteria.

Dosing

Adult

100 mg PO/IV q12h

Pediatric

<8 years: Not recommended
>8 years: 1 mg/kg PO/IV q12h; not to exceed 200 mg/d

Interactions

Minimal decrease in bioavailability with antacids containing aluminum, calcium, magnesium, iron, or bismuth subsalicylate

Contraindications

Documented hypersensitivity; severe hepatic dysfunction

Precautions

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Photosensitivity may occur with prolonged exposure to sunlight or tanning equipment; reduce dose in renal impairment; consider drug serum level determinations in prolonged therapy; if used during tooth development (last half of pregnancy through age 8 y), can cause permanent discoloration of teeth; Fanconilike syndrome may occur with tetracyclines past expiration date


Clindamycin (Cleocin)

Alternative in patients allergic to penicillin. Lincosamide agent that inhibits bacterial growth, possibly by blocking dissociation of peptidyl t-RNA from ribosomes, causing RNA-dependent protein synthesis to arrest. Drawback is lack of coverage against some companion bacteria.

Dosing

Adult

600 mg IV q8h
Alternatively, 150-300 mg PO q8h

Pediatric

8-20 mg/kg/d as hydrochloride or 8-25 mg/kg/d as palmitate PO divided tid/qid
20-40 mg/kg/d IV divided tid/qid

Interactions

Increases duration of neuromuscular blockade induced by tubocurarine and pancuronium; erythromycin may antagonize effects; antidiarrheals may delay absorption

Contraindications

Documented hypersensitivity; regional enteritis; ulcerative colitis; hepatic impairment; antibiotic-associated colitis

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Adjust dose in severe hepatic dysfunction; no adjustment necessary in renal insufficiency; associated with severe and possibly fatal colitis


Amoxicillin/clavulanic acid (Augmentin)

Drug combination that can be used alone in mild to moderately severe cases of actinomycosis; covers both pathogenic actinomycetes and companion bacteria, which frequently are resistant to penicillin.

Dosing

Adult

500 mg PO q8h or 875 mg PO q12h

Pediatric

<40 kg: 20-40 mg/kg/d PO divided bid
>40 kg: Administer as in adults

Interactions

Coadministration with warfarin or heparin increases risk of bleeding

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Caution with renal impairment since drug eliminated via renal mechanisms; adjust dosage when CrCl <30 mL/min


Ceftriaxone (Rocephin)

Covers both pathogenic actinomycetes and companion bacteria, which frequently are resistant to penicillin. Useful in moderately severe to severe forms of cervicofacial and thoracic actinomycosis. Third-generation cephalosporin with broad-spectrum, gram-negative activity; lower efficacy against gram-positive organisms. Arrests bacterial growth by binding to penicillin-binding proteins.

Dosing

Adult

2 g IV/IM q12-24h; not to exceed 4 g/d

Pediatric

Neonates >7 d: 25-50 mg/kg/d IV/IM; not to exceed 125 mg/d
Infants and children: 100 mg/kg/d IV/IM divided q12h; not to exceed 2 g/d

Interactions

Probenecid may increase levels; coadministration with ethacrynic acid, furosemide, and aminoglycosides may increase nephrotoxicity

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Adjust dose in renal impairment; caution in breastfeeding women, allergy to penicillin, pseudo-biliary lithiasis, and non— C difficile diarrhea


Imipenem/cilastatin (Primaxin)

Covers both pathogenic actinomycetes and companion bacteria, which frequently are resistant to penicillin. Useful in moderately severe to severe forms of abdominal and pelvic actinomycosis.

Dosing

Adult

500-1000 mg IV q8h, not to exceed 4 g/d

Pediatric

Not established; 15-25 mg/kg/dose IV q6h suggested for >3 mo

Interactions

Coadministration with cyclosporine may increase CNS adverse effects of both agents; coadministration with ganciclovir may result in generalized seizures

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Adjust dose in renal insufficiency; avoid use in children <12 years

Follow-up

Further Inpatient Care

  • Obtain imaging studies and percutaneous diagnostic studies to allow more expedient diagnosis of actinomycosis.
  • Place a peripherally inserted central catheter (PICC) for administration of intravenous antibiotics.
  • Arrange outpatient intravenous antibiotic therapy.
  • If penicillin therapy is failing, consider broadening the antimicrobial spectrum to cover the potentially uncultured companion bacteria.

Further Outpatient Care

  • Follow up on outpatient intravenous antibiotic programs and switch patients to oral antibiotic therapy. Prolonged antibiotic therapy is often required.
  • Use CT scanning and MRI to monitor the response to therapy.

Inpatient & Outpatient Medications

  • Parenteral antibiotics are administered initially via PICC line, with transition to oral agents.

Transfer

  • If a CT scanner or interventional radiology is not available, transfer to a facility with these services.

Deterrence/Prevention

  • Maintenance of good oral hygiene and adequate regular dental care are important.
  • Patients and physicians alike should be aware of the increased risk of infection associated with insertion of IUCD.

Complications

  • Osteomyelitis of the mandible, ribs, and vertebrae
  • CNS disease, including brain abscess; chronic meningitis; actinomycetoma; cranial, epidural, and subdural infection; and spinal epidural infection
  • Endocarditis
  • Hepatic actinomycosis
  • Disseminated actinomycosis

Prognosis

  • When actinomycosis is diagnosed early and treated with appropriate antibiotic therapy, the prognosis is excellent.
  • The more advanced and complicated actinomycotic forms require aggressive antibiotic and surgical therapy for optimal outcome; however, deaths can occur despite such therapy.

Patient Education

  • Because actinomycosis is an endogenous infection, no risk of person-to-person transmission exists.

Miscellaneous

Medicolegal Pitfalls

  • Failure to make a timely diagnosis: To minimize delays in diagnosis, actinomycosis should be considered in the differential diagnoses of any inflammatory lesion of subacute or long-term nature.
  • Failure to determine ineffectiveness of antibiotic therapy

Multimedia

Actinomycosis in the endometrial tissue, low-powe...

Media file 1: Actinomycosis in the endometrial tissue, low-power view. Image courtesy of Paul Gibbs, MD.

Actinomycosis in the endometrial tissue, high-pow...

Media file 2: Actinomycosis in the endometrial tissue, high-power view. Image courtesy of Paul Gibbs, MD.

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Keywords

actinomycosis, cervicofacial actinomycosis, thoracic actinomycosis, abdominal actinomycosis, pelvic actinomycosis, Actinomyces israeli, Actinomyces gerencseriae, Actinomyces naeslundii, Actinomyces odontolyticus, Actinomyces viscosus, Actinomyces turicensis, Actinomyces meyeri, A israeli, A gerencseriae, A naeslundii, A odontolyticus, A viscosus, A turicensis, A meyeri, Propionibacterium propionicus, Actinobacillus actinomycetemcomitans, Prevotella, Fusobacterium, Bacteroides, Staphylococcus, Streptococcus, Enterobacteriaceae, actinomycetes, actinophytosis, lumpy jaw, hepatic actinomycosis, disseminated actinomycosis

Contributor Information and Disclosures

Author

Jason F Okulicz, MD, Assistant Professor of Medicine, Uniformed Services University of the Health Sciences; Staff, Infectious Disease Service, Brooke Army Medical Center
Jason F Okulicz, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians-American Society of Internal Medicine, and Infectious Diseases Society of America
Disclosure: Nothing to disclose.

Coauthor(s)

Hari Polenakovik, MD, Consultant Physician in Infectious Diseases and General Medicine, Department of Medicine, Western Health, Australia
Hari Polenakovik, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, and Infectious Diseases Society of America
Disclosure: Nothing to disclose.

Sylvia Polenakovik, MD, Clinical Instructor, Internist, Department of Internal Medicine, Wayne Hospital, Wright State University
Sylvia Polenakovik, MD is a member of the following medical societies: American College of Physicians-American Society of Internal Medicine and American Medical Association
Disclosure: Nothing to disclose.

Medical Editor

Daniel R Lucey, MD, MPH, Chief, Fellowship Program Director, Department of Internal Medicine, Division of Infectious Diseases, Washington Hospital Center; Professor, Department of Internal Medicine, Uniformed Services University of the Health Sciences
Daniel R Lucey, MD, MPH is a member of the following medical societies: Alpha Omega Alpha and American College of Physicians
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Joseph F John Jr, MD, FACP, FIDSA, FSHEA, Clinical Professor of Medicine, Molecular Genetics and Microbiology, Medical University of South Carolina; Associate Chief of Staff for Education, Ralph H Johnson Veterans Affairs Medical Center
Disclosure: BioMerieux Honoraria Review panel membership; Cubist Honoraria Review panel membership; Pfizer Honoraria Speaking and teaching; Merck Stock dividends stock holdings

CME Editor

Eleftherios Mylonakis, MD, Clinical and Research Fellow, Department of Internal Medicine, Division of Infectious Diseases, Massachusetts General Hospital
Eleftherios Mylonakis, MD is a member of the following medical societies: American Association for the Advancement of Science, American College of Physicians, American Society for Microbiology, and Infectious Diseases Society of America
Disclosure: Nothing to disclose.

Chief Editor

Burke A Cunha, MD, Professor of Medicine, State University of New York School of Medicine at Stony Brook; Chief, Infectious Disease Division, Winthrop-University Hospital
Burke A Cunha, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, and Infectious Diseases Society of America
Disclosure: Nothing to disclose.

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