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Bacterial invasion of pulmonary vessels
Bacterial Invasion of Pulmonary Vessels Pseudomonas Bacteremia Mimicking Pulmonary Thromboembolism with Infarction
ROSEMARY SOAVE, M.D. HENRY W. MURRAY, M.D. MARIA M. LITRENTA, M.D. New York, New York
Pseudomonas aeruginosa displays a curious propensity for invading blood vessels and causing vessel wall necrosis. This bacteremiarelated “vasculitis” is often associated with hemorrhagic necrosis and infarction of surrounding organ parenchyma. With the exception of skin lesions, however, clinical manifestations of Ps. aeruginosa vasculitis seldom occur. In the patient we describe, fatal Ps. aeruginosa bacteremia was first manifested by a syndrome indistinguishable from pulmonary thromboembolism with infarction. Invasion and necrosis of blood vessel walls is a well recognized and distinctive histopathologic feature of bacteremic Pseudomonas aeruginosa infections [ l-l 01. Characteristic lesions (“vasculitis”) may occur in vessels in almost any organ as well as in the aorta and portal vein [7]. In the pulmonary vasculature of patients with Ps. aeruginosa pneumonia, vasculitis correlates pathogenetically- with infection spread hematogenously to the lung. In contrast, pulmonary vascular invasion is not observed in cases of primary Ps. aeruginosa pneumonia in which infection is acquired by aspiration or inhalation
[81. This organism’s propensity for vascular invasion has led to the suggestion that pulmonary involvement in patients with Ps. aeruginosa bacteremia may mimic pulmonary thromboembolism with infarction. However, only one case of this association has apparently been reported [lo]. We report an additional case in which classic pulmonary infarction was the first clinical manifestation of rapidly fatal Ps. aeruginosa bacteremia. This case illustrates the diagnostic confusion which this syndrome may cause and also reemphasizes vascular invasion as an important clinical as well as pathologic manifestation of Ps. aeruginosa infections. CASE REPORT A 42 year old woman with long-standingrheumatic heart disease and systemic
lupus erythernatosus (SE) was hospitalized because of four weeks of fatigue, arthralgias and low grade fever. Two weeks before, maintainence prednisone
FromThe Departmentsof MedicineandPathology, The New York Hospital-CornellMedical Center, New York, New York. Requests for repints should be addressedto Dr. RosemarySoave, 525 East 66th Street. New York. New York 10021. Manuscript accepted May 31 1976.
864
November 1978
therapy (5 rrg/day) was increased to 20 mg/day without improvement. During the 10 days prior to admission, a nonproductive cough developed. Examination revealed a chronically ill-appearing woman in no distress. Abnormal findings were limited to a temperature of 38.2% and previously noted murmurs of mitral stenosis and insufficiency.The white blood cell count was 2,300/mm3 (80 per cent polymorphonuclear leukocytes). Urinalysis revealed 2+ protein and many red cells and red cell casts. A chest x-ray film obtained on admission (Figure 1, left) demonstrated basilar pleural scarring unchanged from a film obtained six months before; decubitus views showed no free pleural fluid. Electrocardiogram revealed sinus rhythm. Sputum gram
The American Journal of Medicine Volume 85
BACTERIAL
INVASION
OF PULMONARY
VESSELS-SOAVE
ET AL.
Figure 1. Chestx-my fill n obtained on ion (left) and after 3nset of pulmonary syktpt6ms showing peripheral infiltrate in the middle lobe of the right iung. (fight).
stain showed few leukocytes and no predominant organism. Six blood cultures obtained over 48 hours were negative as was a urine culture. Sputum culture subsequently grew normal throat flora and scanty Ps. aeruginosa. Active SLE was indicated by hypocomplementemia and the presence of antinuclear and anti-DNA antibodies. Prednisone therapy was increased to 60 mg/day. On the third day, fever with temperature to 39.5”C developed and was accompanied by sudden pleuritic pain in the right side of the chest and shortness of breath. A right pleural friction rub was heard and chest film showed a wedgeshaped, pleural-based right mid-lung field infiltrate (Figure 1, right). The oxygen tension (PO*), with the patient breathing room air was 50 mm Hg, and heparin therapy was begun for presumed pulmonary embolism. An electrocardiogram showed atrial fibrillation. Six hours later, hypotension. oliguria and marked tachypnea developed, and the administration of heparin was discontinued because of initial suspicion of cardiac tamponade. Hypotension persisted despite fluid replacement, and dopamine was given. Rales were subsequently heard throughout both lung fields. Several hours later the patient abruptly became comatose and required mechanical ventilation. New maculopapular and pustular skin lesions were observed. Sputum gram stain showed many gram-negative bacilli, and therapy with clindamycin, tobramycin and carbenicillin was begun. Coagulation studies were consistent with disseminated intravascular coagulation (DIG). A repeat white blood cell count was l,500/mm3 (16 per cent polymorphonuclear leukocytes, 33 per cent band forms, 51 lymphocytes). A chest film showed diffuse bilateral infiltrates. Over the next 24 hours, the patient experienced gastrointestinal bleeding, became increasingly hypoxic, and remained hypotensive and oliguric. Computerized tomographic (CT) scan of the brain disclosed no abnormalities. Despite further therapy with heparin (for DIC) and peritoneal dialysis, the patient died the next day. Cultures of blood, sputum and skin lesion aspirate all grew Ps. aeruginosa sensitive to tobramycin and carbenicillin.
At autopsy, there was evidence of lupus nephritis and stigmata of rheumatic heart disease. Gross examination of the lungs showed areas of patchy consolidation throughout, especially in the middle lobe of the right lung, and numerous bilateral 2 to 4 mm gray-yellow nodules. There was a welldefined, wedge-shaped infarct in the middle lobe of the right lung (Figure 2). Microscopically, extensive bromchopneumonia, microabscess formation and diffuse hemorrhagic necrosis were present. In the middle lobe of the right lung and elsewhere, pulmonary vessels showed gross bacillary invasion and vessel wall necrosis (Figure 3). Bacilli were not intraluminal. In addition, there were metastatic microabscesses in multiple other organs. Vessels in the thyroid, gallbladder, bowel, skin and spinal cord showed necrotic changes and contained numerous gram-negative bacilli.
COMMENTS
This case illustrates several well-recognized features of Ps. aeruginosa bacteremia in an immunocompromised patient. Predisposed by corticosteroid therapy, leukopenia and, perhaps, hypocomplementemia [ 1 I], bacteremia in our patient was overwhelming, rapidly fatal and associated with characteristic skin lesions, DIC and multiple organ seeding. Unusual, however, was the manner in which Ps. aeruginosa bacteremia presented; that is, with pulmonary involvement mimicking bland pulmonary thromboembolism with infarction. Indeed, it is difficult to fault the immediate initiation of heparin therapy in our patient in the face of known predisposition to thromboembolism (bed rest, mitral valve disease) and the textbook-like constellation of symptoms, signs and blood gas, electrocardiographic and chest roentgenographic findings. Only hours later, in the setting of persistent hypotension, marked clinical, deterioration and the appearance of skin lesions, was the diagnosis
November 1978
The American Journal of Medicine
Volume 65
865
BACTERIAL
INVASION
OF PULMONARY
VESSELS-SOAVE
ET AL.
Figure 2. Cut section of the lobe of the right lung showing foci of abscess formation (arrow) and a well-circumscribed, pleural-based infarct {arrowheads).
of septic shock apparent. In retrospect, perhaps fever should have suggested another process besides bland pulmonary embolism with infarction. However, initially low grade fever was attributed to active SLE; at the time of the acute pulmonary event, higher fever was ascribed to pulmonary infarction. Moreover, during the preceding 48 hours, multiple blood cultures and a chest film were negative. Thus, even with hindsight, we have been unable to identify factors which should have raised suspicion of emerging infection and led to empiric antibiotic therapy. Pseudomonas Vasculitis. Ps. aeruginosa bacteremia-induced vascular lesions have a characteristic and striking histopathologic appearance which has been reported in detail [5-71. In the lung, walls of small and medium-sized vessels (both arteries and veins) are directly involved sometimes to massive proportions by invading bacilli. Vessel wall necrosis, necrotizing pneumonitis and hemorrhagic infarction are commonly found [5-71. The inflammatory response to the vascular lesions, however, is curiously minimal or absent. Indeed, it has been proposed that local tissue “neutropenia” may permit bacillary invasion and vasculitis to proceed since, in areas showing a well developed leukocyte response, vessel invasion and necrosis seldom occur [5]. Also characteristic of Ps. aeruginosa vascular lesions is the paucity of both intraluminal bacilli and adjacent intravascular thrombi [5-71. These findings are in contrast to septic pulmonary emboli caused by other bacteria in which the vessel lumen is filled with clot and organisms [lo]. Helpful in explaining the pathogenesis of Ps. aeruginosa vascular lesions is an experimental animal study [5] which demonstrated that the initial site
Figure 3. Small pulmonary artery showing diffuse vessel wall necrosis and bacillary invasion of the media {arrow). Vessel lumen contains unclotted erythrocytes (Cram stain; magnificath X 400, reduced by 25 per cent). Insert (lower right) is a magnification (X 2) of vessel wall adjacent to the arrow. Abundant bacilli are present in the vessel media.
866
November 1978
The American Journal of Medicine
Volume 65
BACTERIAL
of metastatic infection is at the capillary level in tissue surrounding the vessels. Subsequent invasion of vessel walls by Ps. aeruginosa bacilli proceeds centripetally from periphery to center and may, depending upon the stage of infection, become transmural. Adjacent parenchyma is simultaneously involved often showing hemorrhagic necrosis and infarction. These findings have been confirmed in human lungs as well [6,7]. Because vascular invasion is not always found in or adjacent to areas of parenchymal necrosis nor are bacilli consistenly identified in all necrotic vessel walls, it has been suggested that toxic products elaborated by Ps. aeruginosa may also play some role in the pathogenesis of the vasculitic lesions [ 5,6,8, lo]. For reasons which are not clear, blood vessel invasion is apparently not a feature of infections caused by other bacteria. In one study of 33 patients with fatal bacteremia caused by a variety of gram-negative bacilli [7], vascular invasion was found in nine patients. All nine patients had Ps. aeruginosa bacteremia. It should also be pointed out that in patients with mucormycosis and aspergillosis pulmonary vascular invasion may develop. Thus, when caring for immunosuppressed patients in whom pulmonary infarction syndromes develop, fungal infection must also be kept in mind [ 121. Since the lung is frequently involved in patients with fatal Ps. aeruginosa bacteremia [ 131, especially in those with underlying hematologic disorders [7], and
INVASION
OF PULMONARY
VESSELS-SOAK
ET AL.
pulmonary vascular invasion is not uncommon [ 141, it has been suggested that the clinical presentation of Ps. aeruginosa pneumonia caused by hematogenous seeding may mimic that of bland pulmonary embolism with infarction. However, we could find only one other well documented example of this association which occurred in a granulocytopenic patient with lymphoma who died of massive hemoptysis within one day of the onset of pulmonary infarction symptoms [lo]. At autopsy, necrotizing hemorrhagic pneumonia and multiple infarcts were present, and necrotic pulmonary vessel walls contained gram-negative bacilli. With the exception of skin lesions (ecthyma gangrenosum) and the pulmonary infarction presentation, no other clinical manifestations have been attributed antemortem to Ps. aeruginosa vasculitis. Thus, it is not surprising that it remains difficult to suspect a particular gram-negative bacillus on a clinical basis in a septicappearing patient [ 161. However, either of these findings in the appropriate clinical setting should suggest Ps. aeruginosa bacteremia and indicate the need for specific antimicrobial therapy pending culture results and further observation. ACKNOWLEDGMENT We are grateful to Drs. C. Richard Minick and Daniel R. Alonso for help with the pathologic material.
REFERENCES 1. 2. 3.
4.
5. 6.
7.
8.
FrenkelE: Uber die Menschenpathogenitat des Bacillus pyocyaneus. Z Hyg Inf 72: 486, 19 12. Forkner CE, Frei E, Edgcomb JH, Utz JP: Pseudomonas septicemia. Am J Med 25: 877, 1958. Margaretten W. Nakai H, Landing BH: Significance of selective vasculitis and the bone-marrow syndrome in Pseudomonas septicemia. N Engl J Med 265: 773, 1961. Curtin JA, Petersdorf RG, Bennett IL: Pseudomonas bacteremia: review of ninety-one cases. Ann Intern f&d 54: 1007, 1961. Teplitz C: Pathogenesis of Pseudomonas vasculitis and septic lesions. Arch Pathol 80: 297, 1965. Fetzer AE, Werner AS, Hagstrom JWC: Pathologic features of pseudomonal pneumonia. Ann Rev Respir Dis 96: 1121, 1967. McHenry MC, Boggenstoss &H, Martin WJ: Bacteremia due to gram negative bacilli. Clinical and autopsy findings in 33 cases. Am J Clin Pathol 50: 160. 1968. Tillotson JR, Lerner AM: Characteristics of nonbacteremic
9.
10.
11. 12. 13. 14.
15.
November 1978
Pseudomonas Pneumonia. Ann Intern Med 68: 295, 1968. Whitecar JP, Luna M. Bodey GP: Pseudomonas bacteremia in patients with malignant diseases. Am J Med Sci 260: 216, 1970. Fishman LS. Armstrong D: Pseudomonas aeruginosa bacteremia in patients with neoplastic disease. Cancer 30: 764, 1972. Agnello V: Complement deficiency states. Medicine (Baltimore) 57: 1. 1978. Murray HW: Pulmonary mucormycosis: 160 years later. Chest 72: 1, 1977. Baltch AL, Griffin PE: Pseudomonas aeruginosa bacteremia. Am J Med Sci 274: 119, 1977. Pennington JE, Reynolds HY, Carbone PP: Pseudomonas pneumonia. A retrospective study of 36 cases. Am J Med 55: 155. 1973. Flick MFt, Cluff LE: Pseudomonas bacteremia. Review of 108 cases. Am J Med 60: 501, 1976.
The American Journal of Medlclne
Volume 65
867
ROSEMARY SOAVE, M.D. HENRY W. MURRAY, M.D. MARIA M. LITRENTA, M.D. New York, New York
Pseudomonas aeruginosa displays a curious propensity for invading blood vessels and causing vessel wall necrosis. This bacteremiarelated “vasculitis” is often associated with hemorrhagic necrosis and infarction of surrounding organ parenchyma. With the exception of skin lesions, however, clinical manifestations of Ps. aeruginosa vasculitis seldom occur. In the patient we describe, fatal Ps. aeruginosa bacteremia was first manifested by a syndrome indistinguishable from pulmonary thromboembolism with infarction. Invasion and necrosis of blood vessel walls is a well recognized and distinctive histopathologic feature of bacteremic Pseudomonas aeruginosa infections [ l-l 01. Characteristic lesions (“vasculitis”) may occur in vessels in almost any organ as well as in the aorta and portal vein [7]. In the pulmonary vasculature of patients with Ps. aeruginosa pneumonia, vasculitis correlates pathogenetically- with infection spread hematogenously to the lung. In contrast, pulmonary vascular invasion is not observed in cases of primary Ps. aeruginosa pneumonia in which infection is acquired by aspiration or inhalation
[81. This organism’s propensity for vascular invasion has led to the suggestion that pulmonary involvement in patients with Ps. aeruginosa bacteremia may mimic pulmonary thromboembolism with infarction. However, only one case of this association has apparently been reported [lo]. We report an additional case in which classic pulmonary infarction was the first clinical manifestation of rapidly fatal Ps. aeruginosa bacteremia. This case illustrates the diagnostic confusion which this syndrome may cause and also reemphasizes vascular invasion as an important clinical as well as pathologic manifestation of Ps. aeruginosa infections. CASE REPORT A 42 year old woman with long-standingrheumatic heart disease and systemic
lupus erythernatosus (SE) was hospitalized because of four weeks of fatigue, arthralgias and low grade fever. Two weeks before, maintainence prednisone
FromThe Departmentsof MedicineandPathology, The New York Hospital-CornellMedical Center, New York, New York. Requests for repints should be addressedto Dr. RosemarySoave, 525 East 66th Street. New York. New York 10021. Manuscript accepted May 31 1976.
864
November 1978
therapy (5 rrg/day) was increased to 20 mg/day without improvement. During the 10 days prior to admission, a nonproductive cough developed. Examination revealed a chronically ill-appearing woman in no distress. Abnormal findings were limited to a temperature of 38.2% and previously noted murmurs of mitral stenosis and insufficiency.The white blood cell count was 2,300/mm3 (80 per cent polymorphonuclear leukocytes). Urinalysis revealed 2+ protein and many red cells and red cell casts. A chest x-ray film obtained on admission (Figure 1, left) demonstrated basilar pleural scarring unchanged from a film obtained six months before; decubitus views showed no free pleural fluid. Electrocardiogram revealed sinus rhythm. Sputum gram
The American Journal of Medicine Volume 85
BACTERIAL
INVASION
OF PULMONARY
VESSELS-SOAVE
ET AL.
Figure 1. Chestx-my fill n obtained on ion (left) and after 3nset of pulmonary syktpt6ms showing peripheral infiltrate in the middle lobe of the right iung. (fight).
stain showed few leukocytes and no predominant organism. Six blood cultures obtained over 48 hours were negative as was a urine culture. Sputum culture subsequently grew normal throat flora and scanty Ps. aeruginosa. Active SLE was indicated by hypocomplementemia and the presence of antinuclear and anti-DNA antibodies. Prednisone therapy was increased to 60 mg/day. On the third day, fever with temperature to 39.5”C developed and was accompanied by sudden pleuritic pain in the right side of the chest and shortness of breath. A right pleural friction rub was heard and chest film showed a wedgeshaped, pleural-based right mid-lung field infiltrate (Figure 1, right). The oxygen tension (PO*), with the patient breathing room air was 50 mm Hg, and heparin therapy was begun for presumed pulmonary embolism. An electrocardiogram showed atrial fibrillation. Six hours later, hypotension. oliguria and marked tachypnea developed, and the administration of heparin was discontinued because of initial suspicion of cardiac tamponade. Hypotension persisted despite fluid replacement, and dopamine was given. Rales were subsequently heard throughout both lung fields. Several hours later the patient abruptly became comatose and required mechanical ventilation. New maculopapular and pustular skin lesions were observed. Sputum gram stain showed many gram-negative bacilli, and therapy with clindamycin, tobramycin and carbenicillin was begun. Coagulation studies were consistent with disseminated intravascular coagulation (DIG). A repeat white blood cell count was l,500/mm3 (16 per cent polymorphonuclear leukocytes, 33 per cent band forms, 51 lymphocytes). A chest film showed diffuse bilateral infiltrates. Over the next 24 hours, the patient experienced gastrointestinal bleeding, became increasingly hypoxic, and remained hypotensive and oliguric. Computerized tomographic (CT) scan of the brain disclosed no abnormalities. Despite further therapy with heparin (for DIC) and peritoneal dialysis, the patient died the next day. Cultures of blood, sputum and skin lesion aspirate all grew Ps. aeruginosa sensitive to tobramycin and carbenicillin.
At autopsy, there was evidence of lupus nephritis and stigmata of rheumatic heart disease. Gross examination of the lungs showed areas of patchy consolidation throughout, especially in the middle lobe of the right lung, and numerous bilateral 2 to 4 mm gray-yellow nodules. There was a welldefined, wedge-shaped infarct in the middle lobe of the right lung (Figure 2). Microscopically, extensive bromchopneumonia, microabscess formation and diffuse hemorrhagic necrosis were present. In the middle lobe of the right lung and elsewhere, pulmonary vessels showed gross bacillary invasion and vessel wall necrosis (Figure 3). Bacilli were not intraluminal. In addition, there were metastatic microabscesses in multiple other organs. Vessels in the thyroid, gallbladder, bowel, skin and spinal cord showed necrotic changes and contained numerous gram-negative bacilli.
COMMENTS
This case illustrates several well-recognized features of Ps. aeruginosa bacteremia in an immunocompromised patient. Predisposed by corticosteroid therapy, leukopenia and, perhaps, hypocomplementemia [ 1 I], bacteremia in our patient was overwhelming, rapidly fatal and associated with characteristic skin lesions, DIC and multiple organ seeding. Unusual, however, was the manner in which Ps. aeruginosa bacteremia presented; that is, with pulmonary involvement mimicking bland pulmonary thromboembolism with infarction. Indeed, it is difficult to fault the immediate initiation of heparin therapy in our patient in the face of known predisposition to thromboembolism (bed rest, mitral valve disease) and the textbook-like constellation of symptoms, signs and blood gas, electrocardiographic and chest roentgenographic findings. Only hours later, in the setting of persistent hypotension, marked clinical, deterioration and the appearance of skin lesions, was the diagnosis
November 1978
The American Journal of Medicine
Volume 65
865
BACTERIAL
INVASION
OF PULMONARY
VESSELS-SOAVE
ET AL.
Figure 2. Cut section of the lobe of the right lung showing foci of abscess formation (arrow) and a well-circumscribed, pleural-based infarct {arrowheads).
of septic shock apparent. In retrospect, perhaps fever should have suggested another process besides bland pulmonary embolism with infarction. However, initially low grade fever was attributed to active SLE; at the time of the acute pulmonary event, higher fever was ascribed to pulmonary infarction. Moreover, during the preceding 48 hours, multiple blood cultures and a chest film were negative. Thus, even with hindsight, we have been unable to identify factors which should have raised suspicion of emerging infection and led to empiric antibiotic therapy. Pseudomonas Vasculitis. Ps. aeruginosa bacteremia-induced vascular lesions have a characteristic and striking histopathologic appearance which has been reported in detail [5-71. In the lung, walls of small and medium-sized vessels (both arteries and veins) are directly involved sometimes to massive proportions by invading bacilli. Vessel wall necrosis, necrotizing pneumonitis and hemorrhagic infarction are commonly found [5-71. The inflammatory response to the vascular lesions, however, is curiously minimal or absent. Indeed, it has been proposed that local tissue “neutropenia” may permit bacillary invasion and vasculitis to proceed since, in areas showing a well developed leukocyte response, vessel invasion and necrosis seldom occur [5]. Also characteristic of Ps. aeruginosa vascular lesions is the paucity of both intraluminal bacilli and adjacent intravascular thrombi [5-71. These findings are in contrast to septic pulmonary emboli caused by other bacteria in which the vessel lumen is filled with clot and organisms [lo]. Helpful in explaining the pathogenesis of Ps. aeruginosa vascular lesions is an experimental animal study [5] which demonstrated that the initial site
Figure 3. Small pulmonary artery showing diffuse vessel wall necrosis and bacillary invasion of the media {arrow). Vessel lumen contains unclotted erythrocytes (Cram stain; magnificath X 400, reduced by 25 per cent). Insert (lower right) is a magnification (X 2) of vessel wall adjacent to the arrow. Abundant bacilli are present in the vessel media.
866
November 1978
The American Journal of Medicine
Volume 65
BACTERIAL
of metastatic infection is at the capillary level in tissue surrounding the vessels. Subsequent invasion of vessel walls by Ps. aeruginosa bacilli proceeds centripetally from periphery to center and may, depending upon the stage of infection, become transmural. Adjacent parenchyma is simultaneously involved often showing hemorrhagic necrosis and infarction. These findings have been confirmed in human lungs as well [6,7]. Because vascular invasion is not always found in or adjacent to areas of parenchymal necrosis nor are bacilli consistenly identified in all necrotic vessel walls, it has been suggested that toxic products elaborated by Ps. aeruginosa may also play some role in the pathogenesis of the vasculitic lesions [ 5,6,8, lo]. For reasons which are not clear, blood vessel invasion is apparently not a feature of infections caused by other bacteria. In one study of 33 patients with fatal bacteremia caused by a variety of gram-negative bacilli [7], vascular invasion was found in nine patients. All nine patients had Ps. aeruginosa bacteremia. It should also be pointed out that in patients with mucormycosis and aspergillosis pulmonary vascular invasion may develop. Thus, when caring for immunosuppressed patients in whom pulmonary infarction syndromes develop, fungal infection must also be kept in mind [ 121. Since the lung is frequently involved in patients with fatal Ps. aeruginosa bacteremia [ 131, especially in those with underlying hematologic disorders [7], and
INVASION
OF PULMONARY
VESSELS-SOAK
ET AL.
pulmonary vascular invasion is not uncommon [ 141, it has been suggested that the clinical presentation of Ps. aeruginosa pneumonia caused by hematogenous seeding may mimic that of bland pulmonary embolism with infarction. However, we could find only one other well documented example of this association which occurred in a granulocytopenic patient with lymphoma who died of massive hemoptysis within one day of the onset of pulmonary infarction symptoms [lo]. At autopsy, necrotizing hemorrhagic pneumonia and multiple infarcts were present, and necrotic pulmonary vessel walls contained gram-negative bacilli. With the exception of skin lesions (ecthyma gangrenosum) and the pulmonary infarction presentation, no other clinical manifestations have been attributed antemortem to Ps. aeruginosa vasculitis. Thus, it is not surprising that it remains difficult to suspect a particular gram-negative bacillus on a clinical basis in a septicappearing patient [ 161. However, either of these findings in the appropriate clinical setting should suggest Ps. aeruginosa bacteremia and indicate the need for specific antimicrobial therapy pending culture results and further observation. ACKNOWLEDGMENT We are grateful to Drs. C. Richard Minick and Daniel R. Alonso for help with the pathologic material.
REFERENCES 1. 2. 3.
4.
5. 6.
7.
8.
FrenkelE: Uber die Menschenpathogenitat des Bacillus pyocyaneus. Z Hyg Inf 72: 486, 19 12. Forkner CE, Frei E, Edgcomb JH, Utz JP: Pseudomonas septicemia. Am J Med 25: 877, 1958. Margaretten W. Nakai H, Landing BH: Significance of selective vasculitis and the bone-marrow syndrome in Pseudomonas septicemia. N Engl J Med 265: 773, 1961. Curtin JA, Petersdorf RG, Bennett IL: Pseudomonas bacteremia: review of ninety-one cases. Ann Intern f&d 54: 1007, 1961. Teplitz C: Pathogenesis of Pseudomonas vasculitis and septic lesions. Arch Pathol 80: 297, 1965. Fetzer AE, Werner AS, Hagstrom JWC: Pathologic features of pseudomonal pneumonia. Ann Rev Respir Dis 96: 1121, 1967. McHenry MC, Boggenstoss &H, Martin WJ: Bacteremia due to gram negative bacilli. Clinical and autopsy findings in 33 cases. Am J Clin Pathol 50: 160. 1968. Tillotson JR, Lerner AM: Characteristics of nonbacteremic
9.
10.
11. 12. 13. 14.
15.
November 1978
Pseudomonas Pneumonia. Ann Intern Med 68: 295, 1968. Whitecar JP, Luna M. Bodey GP: Pseudomonas bacteremia in patients with malignant diseases. Am J Med Sci 260: 216, 1970. Fishman LS. Armstrong D: Pseudomonas aeruginosa bacteremia in patients with neoplastic disease. Cancer 30: 764, 1972. Agnello V: Complement deficiency states. Medicine (Baltimore) 57: 1. 1978. Murray HW: Pulmonary mucormycosis: 160 years later. Chest 72: 1, 1977. Baltch AL, Griffin PE: Pseudomonas aeruginosa bacteremia. Am J Med Sci 274: 119, 1977. Pennington JE, Reynolds HY, Carbone PP: Pseudomonas pneumonia. A retrospective study of 36 cases. Am J Med 55: 155. 1973. Flick MFt, Cluff LE: Pseudomonas bacteremia. Review of 108 cases. Am J Med 60: 501, 1976.
The American Journal of Medlclne
Volume 65
867