| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
Guest Access | Sign In via User Name/Password
|
|
|
|||||||
Guest Access | Sign In via User Name/Password |
|||||||||
* From the Departments of Pulmonary and Critical Care Medicine (Drs. Sarodia, Erzurum, and Maurer) and Anatomic Pathology (Dr. Farver), The Cleveland Clinic Foundation, Cleveland, OH.
Correspondence to: Janet R. Maurer, MD, FCCP, Head, Section of Lung Transplantation, Department of Pulmonary and Critical Care Medicine, A-90, The Cleveland Clinic Foundation, 9500 Euclid Ave, Cleveland, OH 44195; e-mail: maurerj{at}ccf.org
 |
Introduction |
|---|
 TOP Introduction DiscussionConclusionReferences |
|---|
His WBC count was increased to 17 x 103/µL and his erythrocyte sedimentation rate was 24 mm/h. The findings from the rest of the laboratory examination, including hemoglobin, platelet count, serum chemistry, coagulation profile, room air arterial blood gases, and urine analysis, were normal. Results of antinuclear antibody, cytoplasmic and perinuclear antineutrophilic cytoplasmic antibodies (by enzyme immunoassay and fluorescence tests), fungal serologies (for aspergillosis, histoplasmosis, blastomycosis, and coccidioidomycosis), and tuberculin skin test (with positive anergy panel) also were normal or negative.
Chest radiograph (Figs 1 and 2 ) and CT scan (Fig 3 ) are shown.
|
|
What is the most likely diagnosis?
Diagnosis: Pleuropulmonary actinomycosis.
Histopathologic examination of the tissue from left upper lobe lesion obtained by transbronchial biopsy revealed "inflammatory pseudotumor" ie, organizing pneumonia with marked fibroblastic proliferation and scattered chronic inflammatory cells. No granuloma, carcinoma, or sarcoma was seen. The diagnosis of actinomycosis was confirmed by histopathologic examination showing typical "sulfur granules" (Fig 4 ), and by growth of the organisms on anaerobic microbiological culture of the tissue from the left lung lesion obtained by wedge resection. The tissue culture demonstrated Actinomyces spp, anaerobic Gram-negative bacilli, Gram-positive cocci, and Haemophilus aphrophilus (ß-lactamase negative).
|
|
Discussion |
|---|
|
TOPIntroductionDiscussionConclusionReferences |
|---|
Microbiology
Actinomycosis is a misnomer. It is not caused by fungus, but
rather by bacteria. The bacteria causing actinomycosis are
Gram-positive, nonacid-fast, filamentous, locally invasive,
opportunistic bacteria of Actinomyces spp, a part of normal human oral
flora.9
As these are facultative anaerobic bacteria, their
identification needs a strict anaerobic environment on an enriched
media and observation for approximately 1 week. Hence, the diagnosis of
pulmonary actinomycosis is sometimes difficult, and an open lung biopsy
is necessary for adequate tissue culture. The most common Actinomyces
sp causing human disease is Actinomyces israelii. The
bacteria are isolated from the fluid or tissue from sinus drainage,
BAL, transbronchial biopsy, open lung biopsy, and so forth. Infections
with Actinomyces spp are commonly polymicrobial; 65 to 100% of
patients have more than one organism. Usual concomitant bacteria are
anaerobic streptococci, fusiform bacilli, Haemophilus spp, and various
Gram-negative bacilli.4
5
Clinical Features
Pleuropulmonary infection (18%) is one of the most common
clinical presentations of infection with these bacteria, the other
presentations being cervicofacial (49%) or abdominal and pelvic (23%,
mostly ileocecal and genital).5
Rarely, the infection is
reported to primarily involve other organs including heart, spleen,
liver, brain, urinary tract, or musculoskeletal
system.9
10
Infection in these sites causes a dense
mass-like lesion with compression or local invasion of the surrounding
structures or anatomic barriers including fibrous tissues, cartilages,
and bones. Hence, the clinical presentation resembles that of a
malignancy, and many patients (53 to 67%) have undergone surgical
excision of the lesions with the diagnosis established after
excision.1
3
4
5
6
The following typical clinical features of pleuropulmonary infection were present in our patient.1 2 3 4 5 6 7 8 9 10 He was of young age (typically a patient's age is 15 to 35 years, but it can occur in all ages), male gender (it is two to four times more common than in women), and an otherwise healthy and immunocompetent subject. He had symptoms of dry cough, chest pain, and weight loss for a few months without fever, and an unremarkable physical examination except for two loose teeth with possible gingivitis and poor oral hygiene. The chest radiograph and CT scan showed dense mass-like cavitary lesions with pleural effusion. Anaerobic microbiologic tissue cultures showed Actinomyces spp, along with other anaerobic organisms and Haemophilus spp. Histopathology of the lesions showed typical sulfur granules. He had an excellent response during weeks of therapy with high-dose IV penicillin G.
The clinical presentations of pleuropulmonary infection may also include the presence of fever, expectoration of yellow pus with sulfur granules, pleural effusion (empyema necessitatis), draining chest wall sinus tract (from invasion of pleura, bone, muscle, and skin), extruding sulfur granules, nonspecific interstitial or alveolar infiltrates, fungus ball-type lesions, mediastinal mass, an endobronchial lesion, and spinal cord compression or brachial plexus syndrome from compression by a thoracic lesion.10 11 12
There is no evidence of increased incidence of pulmonary actinomycosis in HIV-infected patients.13 14 Even among patients with HIV infection, actinomyces rarely behaves as a true opportunistic pathogen. Its potential for dissemination in patients with AIDS has not been established, probably because the infection has so far been infrequent.
Radiographic Imaging
In our patient, the chest radiograph (Figs 1
and 2
) showed large,
rounded, dense mass-like infiltrates, one in each upper lobe, with a
small left pleural effusion. CT scan of the chest showed the masses to
be multilobulated and cavitating with a maximum diameter of 5.4 cm on
the right and 4.1 cm on the left (Fig 3)
. Pleural thickening, or small
loculated pleural fluid adjacent to the left lung lesion, and
borderline enlargement of mediastinal lymph nodes were also evident.
|
The characteristic findings1 2 3 6 7 8 on CT scan or chest radiograph in pleuropulmonary actinomycosis include airspace consolidation (75 to 100%); lesions that are mass-like (25 to 67%), multifocal (50%), usually peripheral, not limited to pulmonary segment (75%), and involving the upper lobe (38 to 56%) or lower lobe (25 to 88%); cavitation with a thick irregular wall (27 to 62%), mild enlargement of mediastinal lymph nodes (75%), small pleural effusion or empyema (25 to 62%), smooth localized mild pleural thickening adjacent to the airspace consolidation (50%), and chest wall invasion (12 to 60%).
The radiographic combination of pulmonary consolidation, pleural involvement, and adenopathy may be confused with TB and other granulomatous infections.7 Radiographically, actinomycosis may mimic cancer because it does not limit itself to anatomic borders. Actinomycotic intracavitary lung colonization also has been reported, forming a fungus ball with radiologic features (pulmonary air meniscus) similar to a fungus ball caused by Aspergillus spp.11
Histopathology
A histopathologic characteristic of actinomycosis infection is the
presence of sulfur granules in the lesions (Fig 4)
.9
Grossly these are hard, gritty, yellow or dull white by reflected
light, and light brown, translucent, or refractile by transmitted
light. Microscopically, these are distinctive conglomerate masses of
organisms that appear round or oval and have basophilic or amphophilic
masses with radiating rosette or fringe of eosinophilic clubs on the
surface. When crushed and examined by Gram's stain, these reveal
masses of Gram-positive branching filaments. Another histologic feature
of actinomycosis is an inflammatory pseudotumor, ie,
organizing pneumonia with marked fibroblastic proliferation and
scattered chronic inflammatory cells.
Differential Diagnosis
Pulmonary TB, malignancy (primary lung carcinoma-squamous cell,
metastatic lesions, or lymphoma), and vasculitis (Wegener's
granulomatosis) are the most common diseases considered in the
differential diagnosis of pleuropulmonary actinomycosis because of
similar chronic symptoms and radiographic findings.10
Finally, the diagnosis of actinomycosis is confirmed by histopathologic
and microbiologic study.
Pleuropulmonary actinomycosis may also be confused with other causes of cavitary pulmonary lesions including infections (bacterial, eg, staphylococcal, fungal, mycetoma-fungus ball, nocardiosis, or parasitic), and other diseases such as bullae, cystic bronchiectasis, bronchogenic cyst, bronchopulmonary sequestration, and pulmonary infarcts.
Treatment and Prognosis
Surgical excision of the lesion, which was "the only hope for
the highly fatal pulmonary actinomycosis" before the antibiotic era,
is no longer required since 1941, because antibiotic treatments have
resulted in permanent cure.6
Penicillin G is the treatment of choice for actinomycosis.9 A prolonged course (3 to 12 months) of treatment with large doses (10 to 20 million U/d) administered IV is recommended for the first few weeks. Thereafter, oral therapy with 2 to 4 g/d penicillin V is given for a few months depending on such characteristics of the infection as location and dissemination. Other antibiotics shown to be effective include amoxicillin, clindamycin, tetracycline, doxycycline, erythromycin, cephalexin, sulfadiazine, and streptomycin.9 Ceftriaxone also has recently been shown to be an effective and convenient therapeutic agent for initial parenteral therapy.15 Rapid clinical and radiographic response when pulmonary actinomycosis is treated with isoniazid and rifampin may erroneously reinforce the suspicion of TB.16
Although the infection is polymicrobial, the bacteria other than actinomyces usually do not need additional treatment. Surgical drainage of abscesses or excision of sinus tracts may be required. Prognosis with intensive antibiotic therapy for months (and surgical therapy if required) is usually excellent even in locally invasive or disseminated disease. Mortality is now rare.1 3
|
Conclusion |
|---|
|
TOPIntroductionDiscussionConclusionReferences |
|---|
Received for publication November 30, 1998. Accepted for publication March 11, 1999.
|
References |
|---|
|
TOPIntroductionDiscussionConclusionReferences |
|---|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
