120
Pericardial Actinomycosis: Case Report and Review Terry D. Fife,· Sydney M. Finegold, and TImothy Grennan
From the Department of Internal Medicine, University of California, Davis, Sacramento; Research and Medical Services, I4!terans Administration Medical Center, ~st Los Angeles; the Department of Microbiology and Immunology, UCLA School of Medicine, Los Angeles; and the North Sacramento Kaiser Permanente Hospital, Sacramento, California
Pericardial actinomycosis is rare and frequently goes unrecognized during life, a circumstance due in part to a paucity of clinical manifestations and to a low rate of positivity in cultures. We present a case report of pericardial actinomycosis and a review of 18 other cases reported in the literature since 1950. Possible risk factors include aspiration pneumonia, alcohol abuse, and periodontal disease. Actinomyces may cause purulent pericarditis that evolves into cardiac tamponade or constrictive pericarditis. Clues to the identity of the causative organism (e.g., draining sinus tracts and the presence of sulfur granules) are frequently absent, and cultures often fail to yield the organism. Histologic examination of material obtained by biopsy is often necessary to make the diagnosis. Most cases originate from a thoracopulmonary site of actinomycosis and spread directly to the pericardium. Widespread dissemination to extrathoracic organs is uncommon. Treatment consists of high-dose, long-term antimicrobial therapy as well as drainage of the pericardial space.
Human actinomycosis can be caused by any of five species of the genus Actinomyces or by Propionibacterium propionicus, although the most common causative organism is Actinomyces israelii [1, 2]. Thoracic involvement occurs in 15% to 34 % of cases of actinomycosis, but cardiac involvement is rare [2, 3]. In the 106 cases of cardiac actinomycosis reported heretofore, the pericardium has been the most frequently involved site. In one series, rv80% of cases of cardiac actinomycosis involved the pericardium [4]. Although'there are scattered case reports of pericardial actinomycosis in the literature, the descriptions of the clinical features and management of these cases are brief. The last thorough review of the subject was published in 1944 [4]. Since the advent of the antibiotic era and advances in diagnostic cardiology have occurred since that time, we report the characteristics of 19 cases of pericardial actinomycosis described since 1950.
Case Report A 41-year-old woman was well until May 1987, when she developed right-sided pleuritic chest pain. A chest radiograph showed a right-middle-lobe infiltrate and small, bilateral pleural effusions. She received erythromycin, but her condiReceived for publication 12January 1990and in revised form6 April 1990.
* Present affiliation: Department of Neurology, UCLA School of Medicine, Los Angeles, California. Pleaseaddressrequestsfor reprintsto Dr. TerryD. Fife, ReedNeurological ResearchCenter, 710 Westwood Plaza, Los Angeles, California90024. Reviews of Infectious DIseases 1991;13:120-6 © 1991 by The University of Chicago. All rights reserved. 0162-0886/9 l/l 301-0063$02.00
tion did not improve. Subsequently, an electrocardiogram showed diffuse elevation of the ST segments, a finding consistent with pericarditis, although no pericardial rub was heard. Indomethacin was administered, but the patient returned six days later with progressive dyspnea and weight gain. There was no history of cough, fever, or chills. Her medical history was notable only for a seizure disorder, for which she was treated with mephobarbital. On admission to the hospital, the patient's blood pressure was 88/70 mm Hg, the heart rate was 118, and there was a pulsus paradoxus that encompassed the entire range of pulse pressure. The temperature was 95°P and the respiratory rate was 36. She appeared pale and dyspneic, and anasarca was noted. Examination of the head and neck revealed no abnormalities. The external jugular vein was distended to the angle of the jaw when the trunk was elevated to 45°. No adenopathy was present. Chest examination revealed dullness in the lower half of both lung fields. The heart rhythm was regular and there was no murmur, gallop, or rub. There was prominent hepatomegaly; the liver had a span of 17 em at the midclavicular line. The spleen tip was also palpable. Peripheral cyanosis was noted, and the pedal pulses were diminished. Laboratory studies performed on admission revealed the following values: white blood cells, 20,100/mm 3 (70% segmented neutrophils, 4 % band neutrophils, 12% lymphocytes, and 5% monocytes); hematocrit, 27.0%; sodium, 128 mmollL; potassium, 5.9 mmollL; C~, 10 mmollL; lactate dehydrogenase, 1,860 U/L; and creatine phosphokinase, 12 U/L. The chest radiograph (figure 1) showed bilateral pleural effusions. An echocardiogram revealed a large pericardial effusion without right atrial or ventricular collapse (figure 2). Bilateral thoracentesis yielded sterile transudative effusions
RID 1991;13 (January-February)
Pericardial Actinomycosis
121
Figure 1. A radiograph of the chest obtained on admission shows bilateral pleural effusions.
Figure 2. An echocardiograrn obtained 3 days after admission shows a large pericardial effusion.
that were negative for acid-fastbacteria. An abdominal ultrasonogram revealed ascites and hepatomegaly. On the third day of hospitalization, increasing azotemia and rapidly reaccumulating effusions in the pleural spaces were noted, and endotracheal intubation was required due to respiratory failure. Her blood pressure decreased to 80/66 mm Hg, and catheterization of the right heart indicated a pulmonary capillary wedge pressure of 17 em H2O. After pericardiocentesis, which yielded 80 mL of thick, whitish-yellow pus, the blood pressure immediately rose to 100170 mm Hg andthepulmonary capillarywedge pressurepromptly dropped to 12- em H2O. A pericardial catheter and bilateral chest tubes were left in place for continuous drainage. Laboratory studies of the pericardial fluid revealed 10,000 red blood cells/mm? and 326,000 white blood cells/rum", with 99 % polymorphonuclear leukocytes; a protein level of 4.1 gldL; and a lactate dehydrogenase concentration of >12,000 VlL. A gram stain showed only whiteblood cells; no acid-fastbacteria were seen on numerous specimens of pleural and pericardial fluid. The resultsof subsequent culturesofpleural and pericardial fluid were all negative. Treatmentwith antituberculous medicationsand cefotaximehad been initiated 3 days before the culture was obtained. On the fifth day, computed axial tomography of the chest showed a homogenous soft tissue mass, which measured 5 em by 6 em, near the right lowerlobe adjacentto the mediastinum. There wasno evidenceof mediastinallymphadenopathy. After an attempted needle biopsy was unsuccessful, an excisional biopsy of the soft tissue mass was performed on the sixth day. At the time of surgery, the mass appeared as gray necrotic material. Histologically, the tissuehad microabscessestypicalof actinomycosis; the abscessescontained sulfur granules composed of gram-positive, thin, filamentous branching rods with peripheral clubbing. The gram-positive
rodswerehighlighted byGrocott-Gomori methenamine-silver nitrate and Brown and Brenn gram stains (figures 3 and 4). Subsequently, cultures yielded only a few small colonies of Propionibacterium acnes, an organism that was considered a contaminant. Drainage gradually diminished from the pericardial and thoracostomy tubes, and they were removed after 1 week. Treatmentwas begun with penicillin G (3 million U iv every four hours). A Hickman catheter was placed for continued outpatient administration of iv penicillin. The patient recovered completely; follow-up has continued for 3 years.
Methods A search of the literature from 1January 1950to 1January 1990 yielded 28 published reports of cardiac actinomycosis. Inclusion in this review was determined by several criteria: (1) actinomycotic infection, diagnosed either by positivity of culturesof specimens from the infectedarea or by the presence of classic sulfur granules composed of gram-positive branching rods; (2) evidenceof pericardial infectionrelated , to the actinomycotic infection; and (3) an adequate description of the clinical course and physical examination. By these criteria, ten cases of cardiac actinomycosis were excluded: four cases involved the endocardium but not the pericardium [5-8], and six cases were not described in sufficient detail to permit analysis [9-14]. Another case excluded was one of endocarditis that was due to "Actinomyces muris," a gram-negative bacillus nowknown as Streptobacillus moniliformis, and hence was not a genuine case of actinomycosis [15] . Twocases were included eventhoughsulfur granules were not specifically mentioned and no Actinomyces were cultured [16, 17].
Fife, Finegold, and Grennan
122
Figure 3. In this photomicrograph, a tangle of gram-positive, filamentous organisms in the form of a sulfur granule has the morphological appearance of Actinomyces (Brownand Brenn gram stain, x 375).
Results
Tables 1 and 2 list the features of 19 cases of pericardial actinomycosis. The patients'ages ranged from 24 to 57 years, with a mean age of 43 years. Sixteen (84 %) were males, a fact consistent with the previously reported and unexplained predominance of males among persons with actinomycosis [2]. None of the patients had preexisting malignancy or immune suppression, and none of the women had used intrau-
RID 1991;13 (January-February)
Figure 4. A high-powered photomicrograph of a sulfur granule from a specimen of the right lung mass obtained by biopsy (Brown and Brenn gram stain, x 1,500).
terine devices. Three patients(16%) werealcoholics,and five (26 %) had periodontal disease. Fever was often absent at the time of initial presentation, but 13 (68 %) had fever at some point in their clinical course. Six patients (32 %) developed a pericardial friction rub. A primary thoracic focus of infection was identified in 15 subjects (79%), while four had no identifiable contiguous site of infection. Cardiac tamponade developed in 10 patients (53%), and constrictive or adhesive
Table 1. Review of 19 cases of actinomycosis of the pericardium. RefAge (y)1 erence sex
Primary site of infection
Cardiac tamponade
(18) (19) (20) (20) (20) (21) (22) (23)
41/M 351M 381M 57/M 391M 5 liM 321M 47/M
Right chest nodule Left chest abscess Right chest mass Mediastinal mass Right lower lung Right chest abscess Right lower lung Left lower lung
No Yes Yes Yes No No No Yes
[24) (25)
511F 47/M
Unknown Left upper lung
Yes No
(26) (27) (28) (29) [301 (31)
24/F 56/M 381M 43/M 49/M 5 liM
Unknown Unknown Right chest mass Left chest mass Right lung mass Jaw, arm , buttocks
Yes Yes No Yes No No
[16)
361M 56/M 41/F
Left chest mass Right lung Right lung mass
Yes No Yes
(17)
[PRJ NOTE.
NS
= not stated; PR = present report .
Isolate from cultured specimen A. bovis from chest nodule" A. bovis from sinus tract" None NS NS Actinomyces from pericardial abscess None "Fusobacterium fusiforme"t from pericardial fluid None A. israelii from pericardial biopsy specimen NS None None A. israelii from pericardial fluid None Eikenella corrodens , Staphylococcus epidermidis None Fusobacterium nucleatum from blood P. ames
Procedure
Outcome
None Pericardiectomy None None None None None Pericardiectomy
Recovered Recovered Died Died Died Died Recovered Died
Pericardiectomy Pericardiectomy
Recovered Died
Pericardiectomy Pericardiectomy None Pericardial window, catheterization Thoracotomy, pericardiotomy Pericardiectomy
Recovered Died Recovered Recovered Recovered Recovered
Pericardiocentesis None Pericardial catheterization
Recovered Died Recovered
* A. bovis previously was believed to be identical 10 A. israelii, but it is distinct and rarely a pathogen in human actinomycosis; these isolates were probably A. lsraelii. t This is no longer an acceptable genus/species designation.
RID 1991;13 (January-February)
Pericardial Actinomycosis
Table 2. Clinical features reported in 19 cases of pericardial actinomycosis. Feature Symptoms Dyspnea Cough Fever Chest pain Weight loss Signs Pleural effusion Tachypnea Hepatomegaly Peripheral edema Hypotension or pulse pressure 50 % showed evidence of purulent pericarditis [4]. Actinomyces usually reach the pericardial space by spreading directly from an adjacent thoracic focus of actinomycosis, and in some instances the infection extends to the myocardiumor to the endocardium [4, 32]. This stepwise invasion may account for the greater frequency of pericardial involvement. Risk/actors. There is no clear evidencethat neoplasia [9] or an immunocompromised status [2] is a major risk factor in the developmentof pericardial actinomycosis. None of the 19patients discussedin this review wasseriouslyimmunocom-
123
promised or had malignant tumors, and only one case [21] involved widespread dissemination of Actinomyces to extrathoracicorgans. Whiletheyare not compelling, certaindata are suggestive of a link betweenpericardial actinomycosis and impaired immunity. For instance, most cases of purulent pericarditis caused by organisms other than Actinomyces occur in patients with serious underlying disease or who are immunocompromised [10], and there have been isolated reports of infection due to Actinomyces in patients with immune impairment [33-35]. While humoral and cell-mediated immune factors may not significantlyalter the risk of actinomycoticinfection, certain disruptions in local barrier defenses may. Most cases of thoracic actinomycosisfollow aspiration of oropharyngeal contents. Since Actinomyces are normal commensal inhabitants of the oral cavity, they may gain access to the thorax by this mechanism. The breakdownin local pulmonary defenses that follows aspiration of oral contents is thought to initiate thoracic actinomycosis, and associated bacteria may playa con- . tributory role. None of the 19 patients with pericardial actinomycosis included in this review had any reported history of aspiration, even though 15 (79%) had an intrathoracic focus of infection. Aspiration, however, is frequently overlooked. In any case, the greatestrisk factor forthe development of pericardial actinomycosis is antecedent or concomitantthoracicactinomycosis. Other factors associated with pericardial actinomycosis include dental or periodontal disease, which was noted in six patients, and alcohol abuse, which was noted in three. Twopatients had significantmental illness, and two had a history of trauma to the chest with a blunt instrument. One patient had preexisting exogenous allergic alveolitis. The considerationof dental or periodontal disease as a risk factor for actinomycosis remains controversial; although Actinomyces are normal oral inhabitants, actinomycosis is uncommon. Even edentulous patients are prone to thoracic actinomycosis [36]. If dental or periodontal disease is a risk factor, it may be due to alteration in oral bacterial flora, such as by the aspirationoforganismsassociatedwith Actinomyces. Additionally, there is a small but demonstrable risk of bacteremia due to Actinomyces after dental manipulation [37]. It is this rare instance of actinomycotic bacteremia that imparts some credence to the four cases [24, 26, 27, 31] of pericardial actinomycosis in which the organismpresumably directly seeded the pericardium, an event that resulted in pericarditis. Antecedent aseptic pericarditis due to viral illness or uremia does appear to predispose to pericardial seeding in cases of purulent pericarditis [10]; however, none of the casesreviewed hereinhad a history ofantecedent pericarditis or of dental manipulation. Alcohol abuse mayincrease the risk of developing thoracic and pericardial actinomycosis because it increases the likelihood of aspiration. Alcoholism is associated with purulent pericarditis [10]. The use of intrauterine devicesis associated
124
Fife, Finegold, and Grennan
with pelvic actinomycosis [1], but none of the women in the series we report had a history of use of such devices. Clinicalfeatures. The clinicalmanifestations of pericardial actinomycosis were examined in Cornell and Shookhoff's review of 68 cases of cardiac actinomycosis from 1882to 1944 [4]. Although the authors did not report any cases of cardiac tamponade, 13 (36%) of the 36 cases with direct pericardial involvement had pericardialeffusions, and 10(28%) had overt signs of congestiveheart failure. Becauseof the results of this study, the current belief is that congestiveheart failure is the most common clinical finding in pericardial or cardiac actinomycosisand that cardiac tamponade is rare [19, 25, 29]. Among the 19 cases described since 1950, however, tamponade occurred in 10 (53%), whereas congestiveheart failure was not mentioned in any. In only one casewasan enlarged (400-g) heart noted at autopsy [20]. These data cast doubt upon previous contentions that heart failure commonly results from actinomycotic infection of the heart. There have been no documented instances in which actinomycoticmyocarditisappeared to cause heart failure by altering contractility. Rather, most patients with clinical signs of decreasedvenous return havelikelyhad cardiactamponade, constrictive pericarditis, or, in rare cases such as the one reported by Dutton and Inclan [5], valvular heart disease. Purulent pericarditisdue to organismsother than Actinomyces resultsin cardiac tamponadein 38% of patients, and one-third of appropriately treatedsurvivors mayproceedto develop constrictive pericarditis [38]. Five patients (26%) of those reviewed herein developed significant adhesive or constrictivepericarditis. Hence, likepurulent pericarditisdue to other causes, cardiac tamponade is common and may progress to constrictive'pericarditis, but congestive heart failure due to actinomycosis of the pericardium most likely occurs only rarely, if at all. Diagnosis. Prior to the development of overt symptoms of diminished venous return, actinomycosis of the pericardium maybe insidious. Thischaracteristic distinguishes it from most other causes of purulent pericarditis, which are usually detected in
Pericardial Actinomycosis: Case Report and Review Terry D. Fife,· Sydney M. Finegold, and TImothy Grennan
From the Department of Internal Medicine, University of California, Davis, Sacramento; Research and Medical Services, I4!terans Administration Medical Center, ~st Los Angeles; the Department of Microbiology and Immunology, UCLA School of Medicine, Los Angeles; and the North Sacramento Kaiser Permanente Hospital, Sacramento, California
Pericardial actinomycosis is rare and frequently goes unrecognized during life, a circumstance due in part to a paucity of clinical manifestations and to a low rate of positivity in cultures. We present a case report of pericardial actinomycosis and a review of 18 other cases reported in the literature since 1950. Possible risk factors include aspiration pneumonia, alcohol abuse, and periodontal disease. Actinomyces may cause purulent pericarditis that evolves into cardiac tamponade or constrictive pericarditis. Clues to the identity of the causative organism (e.g., draining sinus tracts and the presence of sulfur granules) are frequently absent, and cultures often fail to yield the organism. Histologic examination of material obtained by biopsy is often necessary to make the diagnosis. Most cases originate from a thoracopulmonary site of actinomycosis and spread directly to the pericardium. Widespread dissemination to extrathoracic organs is uncommon. Treatment consists of high-dose, long-term antimicrobial therapy as well as drainage of the pericardial space.
Human actinomycosis can be caused by any of five species of the genus Actinomyces or by Propionibacterium propionicus, although the most common causative organism is Actinomyces israelii [1, 2]. Thoracic involvement occurs in 15% to 34 % of cases of actinomycosis, but cardiac involvement is rare [2, 3]. In the 106 cases of cardiac actinomycosis reported heretofore, the pericardium has been the most frequently involved site. In one series, rv80% of cases of cardiac actinomycosis involved the pericardium [4]. Although'there are scattered case reports of pericardial actinomycosis in the literature, the descriptions of the clinical features and management of these cases are brief. The last thorough review of the subject was published in 1944 [4]. Since the advent of the antibiotic era and advances in diagnostic cardiology have occurred since that time, we report the characteristics of 19 cases of pericardial actinomycosis described since 1950.
Case Report A 41-year-old woman was well until May 1987, when she developed right-sided pleuritic chest pain. A chest radiograph showed a right-middle-lobe infiltrate and small, bilateral pleural effusions. She received erythromycin, but her condiReceived for publication 12January 1990and in revised form6 April 1990.
* Present affiliation: Department of Neurology, UCLA School of Medicine, Los Angeles, California. Pleaseaddressrequestsfor reprintsto Dr. TerryD. Fife, ReedNeurological ResearchCenter, 710 Westwood Plaza, Los Angeles, California90024. Reviews of Infectious DIseases 1991;13:120-6 © 1991 by The University of Chicago. All rights reserved. 0162-0886/9 l/l 301-0063$02.00
tion did not improve. Subsequently, an electrocardiogram showed diffuse elevation of the ST segments, a finding consistent with pericarditis, although no pericardial rub was heard. Indomethacin was administered, but the patient returned six days later with progressive dyspnea and weight gain. There was no history of cough, fever, or chills. Her medical history was notable only for a seizure disorder, for which she was treated with mephobarbital. On admission to the hospital, the patient's blood pressure was 88/70 mm Hg, the heart rate was 118, and there was a pulsus paradoxus that encompassed the entire range of pulse pressure. The temperature was 95°P and the respiratory rate was 36. She appeared pale and dyspneic, and anasarca was noted. Examination of the head and neck revealed no abnormalities. The external jugular vein was distended to the angle of the jaw when the trunk was elevated to 45°. No adenopathy was present. Chest examination revealed dullness in the lower half of both lung fields. The heart rhythm was regular and there was no murmur, gallop, or rub. There was prominent hepatomegaly; the liver had a span of 17 em at the midclavicular line. The spleen tip was also palpable. Peripheral cyanosis was noted, and the pedal pulses were diminished. Laboratory studies performed on admission revealed the following values: white blood cells, 20,100/mm 3 (70% segmented neutrophils, 4 % band neutrophils, 12% lymphocytes, and 5% monocytes); hematocrit, 27.0%; sodium, 128 mmollL; potassium, 5.9 mmollL; C~, 10 mmollL; lactate dehydrogenase, 1,860 U/L; and creatine phosphokinase, 12 U/L. The chest radiograph (figure 1) showed bilateral pleural effusions. An echocardiogram revealed a large pericardial effusion without right atrial or ventricular collapse (figure 2). Bilateral thoracentesis yielded sterile transudative effusions
RID 1991;13 (January-February)
Pericardial Actinomycosis
121
Figure 1. A radiograph of the chest obtained on admission shows bilateral pleural effusions.
Figure 2. An echocardiograrn obtained 3 days after admission shows a large pericardial effusion.
that were negative for acid-fastbacteria. An abdominal ultrasonogram revealed ascites and hepatomegaly. On the third day of hospitalization, increasing azotemia and rapidly reaccumulating effusions in the pleural spaces were noted, and endotracheal intubation was required due to respiratory failure. Her blood pressure decreased to 80/66 mm Hg, and catheterization of the right heart indicated a pulmonary capillary wedge pressure of 17 em H2O. After pericardiocentesis, which yielded 80 mL of thick, whitish-yellow pus, the blood pressure immediately rose to 100170 mm Hg andthepulmonary capillarywedge pressurepromptly dropped to 12- em H2O. A pericardial catheter and bilateral chest tubes were left in place for continuous drainage. Laboratory studies of the pericardial fluid revealed 10,000 red blood cells/mm? and 326,000 white blood cells/rum", with 99 % polymorphonuclear leukocytes; a protein level of 4.1 gldL; and a lactate dehydrogenase concentration of >12,000 VlL. A gram stain showed only whiteblood cells; no acid-fastbacteria were seen on numerous specimens of pleural and pericardial fluid. The resultsof subsequent culturesofpleural and pericardial fluid were all negative. Treatmentwith antituberculous medicationsand cefotaximehad been initiated 3 days before the culture was obtained. On the fifth day, computed axial tomography of the chest showed a homogenous soft tissue mass, which measured 5 em by 6 em, near the right lowerlobe adjacentto the mediastinum. There wasno evidenceof mediastinallymphadenopathy. After an attempted needle biopsy was unsuccessful, an excisional biopsy of the soft tissue mass was performed on the sixth day. At the time of surgery, the mass appeared as gray necrotic material. Histologically, the tissuehad microabscessestypicalof actinomycosis; the abscessescontained sulfur granules composed of gram-positive, thin, filamentous branching rods with peripheral clubbing. The gram-positive
rodswerehighlighted byGrocott-Gomori methenamine-silver nitrate and Brown and Brenn gram stains (figures 3 and 4). Subsequently, cultures yielded only a few small colonies of Propionibacterium acnes, an organism that was considered a contaminant. Drainage gradually diminished from the pericardial and thoracostomy tubes, and they were removed after 1 week. Treatmentwas begun with penicillin G (3 million U iv every four hours). A Hickman catheter was placed for continued outpatient administration of iv penicillin. The patient recovered completely; follow-up has continued for 3 years.
Methods A search of the literature from 1January 1950to 1January 1990 yielded 28 published reports of cardiac actinomycosis. Inclusion in this review was determined by several criteria: (1) actinomycotic infection, diagnosed either by positivity of culturesof specimens from the infectedarea or by the presence of classic sulfur granules composed of gram-positive branching rods; (2) evidenceof pericardial infectionrelated , to the actinomycotic infection; and (3) an adequate description of the clinical course and physical examination. By these criteria, ten cases of cardiac actinomycosis were excluded: four cases involved the endocardium but not the pericardium [5-8], and six cases were not described in sufficient detail to permit analysis [9-14]. Another case excluded was one of endocarditis that was due to "Actinomyces muris," a gram-negative bacillus nowknown as Streptobacillus moniliformis, and hence was not a genuine case of actinomycosis [15] . Twocases were included eventhoughsulfur granules were not specifically mentioned and no Actinomyces were cultured [16, 17].
Fife, Finegold, and Grennan
122
Figure 3. In this photomicrograph, a tangle of gram-positive, filamentous organisms in the form of a sulfur granule has the morphological appearance of Actinomyces (Brownand Brenn gram stain, x 375).
Results
Tables 1 and 2 list the features of 19 cases of pericardial actinomycosis. The patients'ages ranged from 24 to 57 years, with a mean age of 43 years. Sixteen (84 %) were males, a fact consistent with the previously reported and unexplained predominance of males among persons with actinomycosis [2]. None of the patients had preexisting malignancy or immune suppression, and none of the women had used intrau-
RID 1991;13 (January-February)
Figure 4. A high-powered photomicrograph of a sulfur granule from a specimen of the right lung mass obtained by biopsy (Brown and Brenn gram stain, x 1,500).
terine devices. Three patients(16%) werealcoholics,and five (26 %) had periodontal disease. Fever was often absent at the time of initial presentation, but 13 (68 %) had fever at some point in their clinical course. Six patients (32 %) developed a pericardial friction rub. A primary thoracic focus of infection was identified in 15 subjects (79%), while four had no identifiable contiguous site of infection. Cardiac tamponade developed in 10 patients (53%), and constrictive or adhesive
Table 1. Review of 19 cases of actinomycosis of the pericardium. RefAge (y)1 erence sex
Primary site of infection
Cardiac tamponade
(18) (19) (20) (20) (20) (21) (22) (23)
41/M 351M 381M 57/M 391M 5 liM 321M 47/M
Right chest nodule Left chest abscess Right chest mass Mediastinal mass Right lower lung Right chest abscess Right lower lung Left lower lung
No Yes Yes Yes No No No Yes
[24) (25)
511F 47/M
Unknown Left upper lung
Yes No
(26) (27) (28) (29) [301 (31)
24/F 56/M 381M 43/M 49/M 5 liM
Unknown Unknown Right chest mass Left chest mass Right lung mass Jaw, arm , buttocks
Yes Yes No Yes No No
[16)
361M 56/M 41/F
Left chest mass Right lung Right lung mass
Yes No Yes
(17)
[PRJ NOTE.
NS
= not stated; PR = present report .
Isolate from cultured specimen A. bovis from chest nodule" A. bovis from sinus tract" None NS NS Actinomyces from pericardial abscess None "Fusobacterium fusiforme"t from pericardial fluid None A. israelii from pericardial biopsy specimen NS None None A. israelii from pericardial fluid None Eikenella corrodens , Staphylococcus epidermidis None Fusobacterium nucleatum from blood P. ames
Procedure
Outcome
None Pericardiectomy None None None None None Pericardiectomy
Recovered Recovered Died Died Died Died Recovered Died
Pericardiectomy Pericardiectomy
Recovered Died
Pericardiectomy Pericardiectomy None Pericardial window, catheterization Thoracotomy, pericardiotomy Pericardiectomy
Recovered Died Recovered Recovered Recovered Recovered
Pericardiocentesis None Pericardial catheterization
Recovered Died Recovered
* A. bovis previously was believed to be identical 10 A. israelii, but it is distinct and rarely a pathogen in human actinomycosis; these isolates were probably A. lsraelii. t This is no longer an acceptable genus/species designation.
RID 1991;13 (January-February)
Pericardial Actinomycosis
Table 2. Clinical features reported in 19 cases of pericardial actinomycosis. Feature Symptoms Dyspnea Cough Fever Chest pain Weight loss Signs Pleural effusion Tachypnea Hepatomegaly Peripheral edema Hypotension or pulse pressure 50 % showed evidence of purulent pericarditis [4]. Actinomyces usually reach the pericardial space by spreading directly from an adjacent thoracic focus of actinomycosis, and in some instances the infection extends to the myocardiumor to the endocardium [4, 32]. This stepwise invasion may account for the greater frequency of pericardial involvement. Risk/actors. There is no clear evidencethat neoplasia [9] or an immunocompromised status [2] is a major risk factor in the developmentof pericardial actinomycosis. None of the 19patients discussedin this review wasseriouslyimmunocom-
123
promised or had malignant tumors, and only one case [21] involved widespread dissemination of Actinomyces to extrathoracicorgans. Whiletheyare not compelling, certaindata are suggestive of a link betweenpericardial actinomycosis and impaired immunity. For instance, most cases of purulent pericarditis caused by organisms other than Actinomyces occur in patients with serious underlying disease or who are immunocompromised [10], and there have been isolated reports of infection due to Actinomyces in patients with immune impairment [33-35]. While humoral and cell-mediated immune factors may not significantlyalter the risk of actinomycoticinfection, certain disruptions in local barrier defenses may. Most cases of thoracic actinomycosisfollow aspiration of oropharyngeal contents. Since Actinomyces are normal commensal inhabitants of the oral cavity, they may gain access to the thorax by this mechanism. The breakdownin local pulmonary defenses that follows aspiration of oral contents is thought to initiate thoracic actinomycosis, and associated bacteria may playa con- . tributory role. None of the 19 patients with pericardial actinomycosis included in this review had any reported history of aspiration, even though 15 (79%) had an intrathoracic focus of infection. Aspiration, however, is frequently overlooked. In any case, the greatestrisk factor forthe development of pericardial actinomycosis is antecedent or concomitantthoracicactinomycosis. Other factors associated with pericardial actinomycosis include dental or periodontal disease, which was noted in six patients, and alcohol abuse, which was noted in three. Twopatients had significantmental illness, and two had a history of trauma to the chest with a blunt instrument. One patient had preexisting exogenous allergic alveolitis. The considerationof dental or periodontal disease as a risk factor for actinomycosis remains controversial; although Actinomyces are normal oral inhabitants, actinomycosis is uncommon. Even edentulous patients are prone to thoracic actinomycosis [36]. If dental or periodontal disease is a risk factor, it may be due to alteration in oral bacterial flora, such as by the aspirationoforganismsassociatedwith Actinomyces. Additionally, there is a small but demonstrable risk of bacteremia due to Actinomyces after dental manipulation [37]. It is this rare instance of actinomycotic bacteremia that imparts some credence to the four cases [24, 26, 27, 31] of pericardial actinomycosis in which the organismpresumably directly seeded the pericardium, an event that resulted in pericarditis. Antecedent aseptic pericarditis due to viral illness or uremia does appear to predispose to pericardial seeding in cases of purulent pericarditis [10]; however, none of the casesreviewed hereinhad a history ofantecedent pericarditis or of dental manipulation. Alcohol abuse mayincrease the risk of developing thoracic and pericardial actinomycosis because it increases the likelihood of aspiration. Alcoholism is associated with purulent pericarditis [10]. The use of intrauterine devicesis associated
124
Fife, Finegold, and Grennan
with pelvic actinomycosis [1], but none of the women in the series we report had a history of use of such devices. Clinicalfeatures. The clinicalmanifestations of pericardial actinomycosis were examined in Cornell and Shookhoff's review of 68 cases of cardiac actinomycosis from 1882to 1944 [4]. Although the authors did not report any cases of cardiac tamponade, 13 (36%) of the 36 cases with direct pericardial involvement had pericardialeffusions, and 10(28%) had overt signs of congestiveheart failure. Becauseof the results of this study, the current belief is that congestiveheart failure is the most common clinical finding in pericardial or cardiac actinomycosisand that cardiac tamponade is rare [19, 25, 29]. Among the 19 cases described since 1950, however, tamponade occurred in 10 (53%), whereas congestiveheart failure was not mentioned in any. In only one casewasan enlarged (400-g) heart noted at autopsy [20]. These data cast doubt upon previous contentions that heart failure commonly results from actinomycotic infection of the heart. There have been no documented instances in which actinomycoticmyocarditisappeared to cause heart failure by altering contractility. Rather, most patients with clinical signs of decreasedvenous return havelikelyhad cardiactamponade, constrictive pericarditis, or, in rare cases such as the one reported by Dutton and Inclan [5], valvular heart disease. Purulent pericarditisdue to organismsother than Actinomyces resultsin cardiac tamponadein 38% of patients, and one-third of appropriately treatedsurvivors mayproceedto develop constrictive pericarditis [38]. Five patients (26%) of those reviewed herein developed significant adhesive or constrictivepericarditis. Hence, likepurulent pericarditisdue to other causes, cardiac tamponade is common and may progress to constrictive'pericarditis, but congestive heart failure due to actinomycosis of the pericardium most likely occurs only rarely, if at all. Diagnosis. Prior to the development of overt symptoms of diminished venous return, actinomycosis of the pericardium maybe insidious. Thischaracteristic distinguishes it from most other causes of purulent pericarditis, which are usually detected in
