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Radiological Case of the Month
Aisha Jameel, MD;
Stephen Wadowski, MD;
Rona Orentlicher, MD;
Virginia Anderson, MD
From the Department of Pediatrics, Mount Sinai Medical Center (Dr Jameel),
New York City, and the Departments of Pediatrics (Dr Wadowski), Radiology
(Dr Orentlicher), and Pathology (Dr Anderson), SUNY Health Science Center
at Brooklyn, Brooklyn, NY.
Arch Pediatr Adolesc Med. 2001;155:1171-1172.
A 14-YEAR-OLD girl had severe, sharp mid-back pain for 3 weeks and nontender,
gradually enlarging left chest wall swelling for 2 weeks. It was unrelieved
by change of position. One month before symptoms started, she had fallen,
striking her left chest. No bruise remained and the tenderness subsided; however,
2 weeks later, swelling began in the area of injury. She had lost 10 pounds
over the last 2 months while dieting. She had no fever, cough, chills, sweats,
joint pain, or rash. Last year, she lost a filling from a right upper molar,
but otherwise, her last dental care was 6 years ago. She was receiving 325
mg of ferrous sulfate per day for iron deficiency anemia diagnosed 1 month
earlier. Findings from physical examination revealed an obese female (height,
139.7 cm; weight, 83.3 kg). Her temperature was 38.5°C; pulse, 120 beats
per minute; respirations, 20 breaths per minute; and blood pressure, 122/88
mm Hg. Spinal examination showed scoliosis but no vertebral or costal tenderness.
A 4-cm mass was palpated over the left rib cage at the anterior axillary line
in the 10th interspace. This mass was ovoid, nontender, soft, and cool to
the touch without erythema. A large cavity was present in the upper left molar.
Laboratory results included hemoglobin, 5.9 g/dL; hematocrit, 21.2%;
mean corpuscular volume, 67.4 fL; red cell distribution width, 18.6%; reticulocyte
count, 2.6%; prothrombin time, 16 seconds; and partial thromboplastin time,
33 seconds. Chest radiograph showed scoliosis of the lower thoracic and upper
lumbar spine, cardiomegaly, a retrocardiac consolidation, and left pleural
effusion. Fine-needle aspiration of the chest wall mass yielded 20 mL of purulent
material; the chest wall abscess was incised and drained. Serum iron was 10
µg/dL; total iron binding capacity, 159 µg/dL; and ferritin, 397.2
ng/mL. Erythrocytes were hypochromic and microcytic, and the neutrophils had
toxic granules. Erythrocyte sedimentation rate was greater than 140 mm/h.
The rheumatoid factor was positive, and IgG and IgM were increased to 2234
mg/dL and 627 mg/dL, respectively.
Treatment was started with antimicrobials, analgesics for back pain,
and vitamin K injections for prolonged prothrombin time. The prothrombin time
remained prolonged despite vitamin K administration and infusion of fresh
frozen plasma. Anticardiolipin antibody was positive. Routine cultures from
the abscess grew no organisms. The tuberculin skin test result was negative,
and an anergy panel was positive. Computed tomography (CT) of the chest and
abdomen (Figure 1), lateral radiography
(Figure 2), and then magnetic resonance
imaging scan of the spine were performed. A CT-guided biopsy of the paraspinal
mass was performed. Pathologic findings are shown in Figure 3 and Figure 4.
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Figure 1.
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Figure 2.
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Figure 3.
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Figure 4.
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Denouement and Discussion: Thoracic Actinomyces
Figure 1. Midabdominal computed tomographic scan demonstrates destruction of
the T12 vertebra with adjacent left paravertebral soft tissue mass causing
lateral displacement of the left kidney. At the same level, note the large
left chest wall mass with an intra-abdominal component.
Figure 2. Lateral spine radiograph shows T12 vertebral body collapse with adjacent
irregularities of vertebrae T11 and L1.
Figure 3. Medium-power hematoxylin-eosin stain demonstrates fibrous connective
tissue with extensive inflammatory reaction.
Figure 4. Gomori methenamine silver stain of actinomyces granule.
Actinomyces are branching, filamentous, gram-positive, microaerophilic
anaerobes that are normal commensals of the mouth and tonsillar crypts.1 Sulfur granules commonly associated with actinomyces
are suggestive of the organism.2 Microscopically,
the sulfur granule is a colony of organisms.1 Staphylococcus aureus, Nocardia
species, Actinomadura madurae, and some Streptomyces species may produce colonies resembling sulfur granules
(Figure 3 and Figure 4).3 Diagnosis is made
by identifying branching filament colonies.2
Special staining and anaerobic culture techniques help confirm diagnosis since
cultures are positive in only 24% of cases2;
diagnosis is often based on histopathologic findings.
Actinomyces produce focal granulomatous disease with abscess formation. Actinomyces israelii is the most common pathogen, though
other species (Actinomyces meyeri) can cause disease.
It advances by contiguous spread and disregards tissue planes.1
The 3 major forms are cervicofacial (65%), thoracic (15%), and abdominal (20%).4 Cervicofacial disease is from infection of the
teeth and gingiva; abdominal disease may be from perforation of the appendix
or cecum.1 Pulmonary actinomycosis occurs
from aspiration of infected material from the oral cavity or carriage into
the lung by a foreign body, hematogenous seeding, or spread of cervicofacial
or abdominal infection through tissue planes.4
Thoracic actinomycosis often involves pulmonary, pleural, and chest wall tissue
disease.4 Pericardial involvement occurs
in few cases (<2%).5 Pericarditis with
pleural effusion is the most common manifestation.5
Possible aspiration of oral secretions may have been the cause of lung
infection in our patient, spreading to the pericardium, pleura, paraspinal
region, and the T12 vertebra. The paraspinal infection extended to the epidural
space through intervertebral foramina. Lateral spread along a track at the
costal margin resulted in the subcutaneous abscess. Posttraumatic actinomycosis
has been described, but trauma is usually coincidental.3
Vertebral actinomycosis is a chronic febrile illness, with back pain, weight
loss, malaise, and draining sinuses or subcutaneous abscesses.6
Paravertebral abscesses are adjacent to the involved vertebrae and cause spread
to bone.6 The bacterium invades the transverse
processes, body, pedicles, laminae, and spinous processes, yet usually spares
the intervertebral disks, distinguishing itself from tuberculosis of the spine.6 Anemia and thrombocytosis are caused by iron deficiency
and chronic inflammation.7
Antibiotic treatment includes penicillin or clindamycin and tetracycline
in case of penicillin allergy.1, 8
Prompt surgical debridement is necessary in the presence of an abscess.1 With proper therapy there is a 90% cure rate.9 Untreated, the mortality rate is 75% to 100%.10
AUTHOR INFORMATION
Accepted for publication July 12, 2000.
Reprints: Stephen Wadowski, MD, SUNY Children's Medical Center of
Brooklyn, Box 49, 450 Clarkson Ave, Brooklyn, NY 11203.
REFERENCES
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1. Moses J, Bonomo GF, Wenlund DE, Halldorddon TS, Connelly JP. Actinomyces in childhood. Clin Pediatr. 1967;6:221-226.
2. Golden N, Cohen H, Weissbrot J, Silverman S. Thoracic actinomycosis in childhood. Clin Pediatr. 1985;24:646-650.
3. Blinkhorn RJ, Strimbu V, Effron D, Spagnuolo PJ. "Punch" actinomycosis causing osteomyelitis of the hand [abstract]. Arch Intern Med. 1988;148:2668-2670.
ABSTRACT
4. Wilson DC, Redmond AOB. An unusual cause of thoracic mass. Arch Dis Child. 1990;65:991-992.
ABSTRACT
5. Schlossberg D, Franco-Jove D, Woodward C, Schulman J. Pericarditis with effusion caused by Actinomyces
israelii. Chest. 1976;69:680-682.
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6. Lane T, Goings S, Fraser DW, Ries K, Pettrozzi J, Abrutyn E. Disseminated actinomyces with spinal cord compression. Neurology. 1979;29:980-982.
7. Armata J, Cyklis R, Scieslicki A. Thrombocythaemia in actinomycosis. Lancet. 1973;2:261.
8. Nelson JD, Herman DW. Oral penicillin therapy for thoracic actinomycosis. Pediatr Infect Dis. 1986;5:594-595.
PUBMED
9. Weese WC, Smith IM. A study of 57 cases of actinomycosis over a 36-year period. Arch Intern Med. 1975;135:1562-1568.
ABSTRACT
10. Wu CY, Li YW. Multifocal thoracic actinomycosis simulating lymphoma. Pediatr Radiol. 1993;23:541-542.
PUBMED
SECTION EDITOR: BEVERLY P. WOOD, MD
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