Bacteremic Acinetobacter (Herellea) Pneumonia with Survival Case Reportt-a
RICHARD J. WALLACE, JR., ROBERT J. AWE, and R. RUSSELL MARTIN 4
SUMMARY __________________________________________ ______________ A case of community-acquired pneumonia with Acinetobacter calcoacetium var. anitratus (Herellea vaginicola) is presented. Initial leukopenia and sparse leukocytes in the sputum, followed by prolonged leukocytosis and fever, were unusual features of this case. The clinical significance and current antimicrobial drug therapy of acinetobacter infections are discussed.
Introduction Bacterial pneumonia remains one of the most important complications associated with chronic alcoholism. Most of these pneumonias are pneumococcal or anaerobic in origin, but occasionally a primary aerobic gram-negative pneumonia occurs (1). These cases are often fatal, especially when associated with leukopenia. With the use of transtracheal aspiration and newer chemotherapeutic agents, more rapid diagnosis and better survival with these gram-negative pneumonias should be possible. This is the report of a case of bacteremic lobar pneumonia (Received in original form December 15, 1975 and in revised form February l!J, 1976) 1 From the Infectious Disease Division, Departments of Medicine, and Microbiology and Immunology, Baylor College of Medicine, Houston, Tex., and the Pulmonary Disease Division of Jefferson Davis Hospital, Department of Medicine, Baylor College of Medicine, Houston, Tex. 2 Supported by NIH Training Grant USPH AI00446-04 1o5. 3 Requests for reprints should be addressed to Richard J. Wallace, Jr., M.D., Department of Medicine, Baylor College of Medicine, 1200 Moursund Avenue, Houston, Tex. 77030. 4 Dr. Martin is supported by a Research Career Development Award, USPH AI 70335-02 from the National Institutes of Health.
with Acinetobacter calcoacetium var. anitratus (Herellea vaginicola), which is an aerobic, nonfermenting, gram-negative organism. Despite the presence of chronic alcoholism and leukopenia, this patient survived with appropriate antimicrobial drugs and supportive therapy. This case represents one of the few reported survivals of a community-acquired or bacteremic pneumonia with this organism. Case Report
The patient was a 50-year-old male alcoholic who was admitted to the hospital on August 1, 1975 with a 5-day history of fever, cough, and shortness of breath, and a 1-day history of confusion. The patient had been in good health most of his life, except for chronic alcohol abuse and several episodes of respiratory tract infections. He had a cumulative cigarette consumption of 30 pack-years but denied chronic sputum production or exertional dyspnea. The patient had been admitted to another hospital on May 28, 1975 for the treatment of acute diverticulitis of the colon. A chest roentgenogram at that time was interpreted as possibly showing a right lower lobe infiltrate. The leukocyte count was normal, and a sputum culture yielded normal throat flora. A 2-day course of low-dose penicillin was given. The patient then felt well until the onset of respiratory symptoms 2 months later. On admission to this hospital, the patient was an alert, but confused man in moderate respiratory distress. Vital signs included: blood pressure, 100/70 mm Hg; temperature, 100• F; pulse,
AMERICAN REVIEW OF RESPIRATORY DISEASE, VOLUME ll3, 1976
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WALLACE, AWE, AND MARTIN
120 per min, and respirations, 36 per min. There was no scleral icterus. The neck was supple. There was dullness to percussion and rales over the right upper lobe. Skin turgor was poor, but there were no skin lesions or clubbing and no signs of chronic liver disease. Neurologic examination revealed a disoriented, confused man who was hallucinating, but with no focal neurologic signs. Laboratory data included hematocrit, 44 per cent; leukocyte count, 2,400 cells per mm3, with 16 per cent polymorphonuclears, 24 per cent band forms, 8 per cent metamyelocytes, and 44 per cent lymphocytes; platelet count, 30,500 per mm3; blood urea nitrogen, 24 mg per 100 ml; creatinine, 1.0 mg per 100 ml; sodium, 121 mEq per liter; potassium, 2.7 mEq per liter; chloride, 86 mEq per liter; carbon dioxide combining power, 15 mEq per liter; prothrombin time, 10.2 sec, with a control of 10.2 sec; serum glutamic oxaloacetic transaminase, 51 units; alkaline phosphatase, 96 units; bilirubin, 0.7 mg per 100 ml; calcium, 6.1 mg per 100 ml; mag-
nesium, l.l mg per 100 mi. The urinalysis showed 2plus protein and 1 to 3 white cells per high-power field. The chest radiograph showed a dense alveolar infiltrate involving anterior and posterior segments of the right upper lobe (figure 1). A transtracheal aspirate on admission yielded a moderately cellular specimen that contained 80 per cent pigmented alveolar macrophages and only 20 per cent polymorphonuclear leukocytes on wet specimen examination. Grain stain showed sheets of gramnegative cocci in singles and pairs, many of them intracellular (figure 2). Bone marrow aspiration revealed a hypocellular specimen with megakaryocytes present. There was marked vacuolization of erythroid and myeloid precursors, with virtual absence of granulocytes beyond the promyelocytic stage. No megaloblastic changes were present. Spinal fluid obtained by lumbar puncture was normal except for a total protein of 130 mg per 100 mi. Antimicrobial drug therapy was begun with 140 mg of gentamicin given intramuscularly every 8 hours (6 mg per kg
Fig. 1. Admission chest roentgenogram showing a dense right upper lobe infiltrate.
BACTEREMIC ACINETOBACTER PNEUMONIA
697
Fig. 2. Gram stain of the tracheal aspirate revealing both alveolar macrophages and polymorpho· nuclear leukocytes. Numerous gram-negative cocci in singles and pairs are present. Many of the organisms are intracellular (original magnification: X 1,000). per day), and 36 g of carbenicillin per day given intravenously. The patient required intubation because of hypoxia, with the chest radiograph showing progressive involvement of the right middle and low· er lobes. The patient's condition then stabilized on medical therapy, and slow, but gradual, improvement occurred during the next 4 weeks. Culture of tracheal aspirate and blood grew only A. calcoacetium var. anitratus (H. vaginicola); identification of both isolates was confirmed at the Texas State
Department of H ealth Laboratories. The organism was susceptible by disc to tetracycline, kanamycin, colistin, gentamicin, and carbenicillin. The minimal inhibitory concentration (MIC) for carbenicillin was 8.0 ,...g per ml; for gentamicin, 1.0 ,...g per ml. While the patient received 140 mg of gentamicin every 8 hours, serum gentamicin concentrations at I and 2 hours after a dose were 3 to 5 times the MIC for acinetobacter, whereas concentrations at 8 hours were usually still greater than the MIC (mean, 1.2
698
WALLACE, AWE, AND MARTIN
p.g per ml). The patient was treated for 2 weeks with gentamicin and carbenicillin, then received oral tetracycline for an additional week. The sputum was positive for acinetobacter on culture and Gram stain for 3 days, then became negative. The patient was leukopenic for 3 days, after which the white blood cell count increased rapidly. It peaked at 17 days at 47,000 cells per mm3 with 90 per cent polymorphonuclear leukocytes, then very slowly decreased. The leukocyte count was increased for the entire 5-week hospitalization, and was still 19,800 cells per mm3 on discharge. The platelet counts returned to normal. The patient was febrile for a total of 4.5 weeks, during which time an extensive examination for metastatic infection, tuberculosis, or carcinoma to explain the prolonged fever was negative. Bronchoscopy performed in the third week of hospitalization was normal, and right upper lobe brushings revealed no bacteria, fungi, or acid-fast organisms in smears or culture. Numerous sputum cytologic studies were negative. All cultures for tuberculosis, including cerebrospinal fluid, sputum, and bronchial washings, were negative, as were fungal serologies. The fever finally resolved without further antimicrobial drug therapy. The chest radiograph showed gradual clearing of the right middle and lower lobe infiltrates. One month after discharge, the right upper lobe infiltrate still persisted, but with significant retraction and loss of volume. At that time, the patient was asymptomatic, had gained 20 pounds since discharge, and his total leukocyte and differential counts had returned to normal. Discussion Acinetobacter are aerobic gram-negative organisms that clinically resemble the enterobacteriaceae. They differ biochemically, however, as they do not ferment carbohydrates. Both H. vaginicola and Mima polymorpha have been reclassified as acinetobacter. (For purposes of this paper, however, references to acinetobacter will refer only to A. calcoacetium var. anitratus, the new name for herellea.) Previous colonization studies have shown that as many as 25 per cent of normal persons harbor acinetobacter on their skin (2), and as many as 7 per cent carry small numbers of organisms in their throat (3). Despite this apparent ubiquity, acinetobacter has been an infrequent clinical isolate and a rare cause of community-acquired disease. Recent reviews have stressed that acinetobacter is becoming a more frequent sputum bacterial isolate, especially in the hospitalized patient who requires ventilatory support. In a recent study reporting respiratory isolates of acinetobacter, 31 of 37 patients had a tracheostomy or an endotracheal tube (4). The facts that in very few cases has the organism been isolated
on initial sputum culture (4, 5), and that acinetobacter has been isolated more frequently from hospital environmental sites than from patients (6), suggest that most isolates are nosocomially acquir~d. Clinical pneumonia has generally been restricted to severely ill patients on ventilatory support. Significant bacteremia with acinetobacter has usually been associated with indwelling venous catheter infections (7, 8) and only rarely with other conditions (9). Many blood isolates have no relationship to clinical disease, and probably represent skin contamination or insignificant bacteremia (4, 5). Only 3 of the previously reported pneumonias with acinetobacter have had associated bacteremia (10-12). There have been 4 well-documented case reports of community-acquired pneumonia with acinetobacter, 3 of which occurred in compromised hosts (10-13). Two of these patients had chronic renal disease, and one of them, like our patient, was an alcoholic. None had leukopenia. Leukopenia with bacterial pneumonias has generally been a poor prognostic sign. With pneumonia due to Streptococcus pneumoniae or klebsiella, the highest mortality has been among patients with leukopenia (14, 15). A common factor in most of these cases has been the presence of alcoholism. Recent studies have suggested that chronic alcohol consumption directly suppresses granulocyte production (16, 17). In the presence of infection, leukopenia develops as diminished granulocyte reserves become depleted. This phenomenon has been documented with infections due to both gram-positive and gram-negative organisms (17) and may be the explanation for the leukopenia in many of the previously noted pneumonias in alcoholics. This patient has the clinical course and laboratory findings of alcohol-induced marrow suppression as described by Liu (16) and McFarland (17). Like many of their cases, the leukopenia was accompanied by thrombocytopenia. The degree and duration of the rebound leukocytosis, however, was greater than that seen in any of their patients. Of interest was the initial paucity of granulocytes in the tracheal aspirate, which constituted less than 20 per cent of the cells on wet specimen examination (18). This persisted until the return of normal peripheral granulocyte counts. At that time, the sputum became purulent for the first time, with conversion to more than 90 per cent polymorphonuclear leukocytes. Antimicrobial drug therapy for severely ill pa-
BACTEREMIC ACINETOBACTER PNEUMONIA
tients with gram-negative pneumonia has usually used combination therapy (19). When Pseudomonas aeruginosa is not suspected, a popular therapeutic regimen has been cephalothin and gentamicin. With a Gram stain or a culture suggesting acinetobacter, initial therapy should probably include an aminoglycoside plus carbenicillin. Acinetobacter is resistant to the cephalosporins but is usually susceptible to carbenicillin. Unlike most enteric organisms, acinetobacter is more likely to be susceptible to kanamycin than to gentam1cm (20). Ultimate choice of antimicrobial drug therapy, as always, must depend on laboratory susceptibility tests of the specific organism. The previous fatal cases of community-acquired pneumonia with acinetobacter were either misdiagnosed or received inadequate antimicrobial drug therapy. None of them received carbenicillin or an adequate cour~e of gentamicin. Better survival in future cases may be possible with more rapid diagnosis and use of better chemotherapeutic agents. Acknowledgment
7.
8.
9.
10.
II.
12.
13.
14.
The writers acknowledge and appreciate the expert secretarial preparation of Phyllis Faulkner. References l. Tillotson, J. R., and Lerner, A. M.: Pneumonias caused by gram-negative bacilli, Medicine (Baltimore), 1966,45,65. 2. Taplin, D., Rebell, G., and Zaias, N.: The human skin as a source of mimae-herellea infections, JAMA, 1963, 186, 952. 3. Rosenthal, S., and Tager, I. B.: Prevalence of gram-negative rods in the normal pharyngeal flora, Ann Intern Med, 1975,83,355. 4. Gardner, P., Griffin, W. B., Swart, M. N., and Kunz, L. J.: Nonfermentative gram-negative bacilli of nosocomial interest, Am J Med, 1970, 48, 735. 5. Robinson, R. G., Garrison, R. G., and Brown, R. W.: Evaluation of the clinical significance of the genus herellea, Ann Intern Med, 1964, 60, 19. 6. Johanson, W. G., Jr., Pierce, A. K., Sanford, J.P., and Thomas, G. D.: Nosocomial respiratory in-
15.
16. 17.
18. 19.
20.
699
fections with gram-negative bacilli, Ann Intern Med, 1972,77, 701. Daly, A. K., Postic, B., and Kass, E. H.: Infections due to organisms of the genus herellea, Arch Intern Med, 1962,110,580. Green, G. S., Johnson, R. H., Jr., and Shively, J. A.: Mimae: Opportunistic pathogens. A review of infections in a cancer hospital, JAMA, 1966,194, 1065. King, 0. H., Copeland, G. D., and Berton, W. M.: Cardiovascular lesions of the mimae organisms, Am J Med, 1963,35,241. Wands, J. R., Mann, R. B., Jackson, D., and Butler, T.: Pneumonia in chronic renal disease, Am Rev Respir Dis, 1973, 108,964. Hammett, J. B.: Death from pneumonia with bacteremia due to mimae tribe bacterium, JAMA, 1968,206,641. Glick, L. M., Moran, G. P., Coleman, J. M., and O'Brien, G. F.: Lobar pneumonia with bacteremia caused by Bacterium anitratum, Am J Med, 1959,27,183. Gardner, D. L., Pines, A., and Stewart, S. M.: Fulminating and fatal pneumonia and septicemia due to Achromobacter anitratus, Br Med J, 1960,1' ll08. Van Metre, T. E.: Pneumococcal pneumonia treated with antibiotics: The prognostic significance of certain clinical findings, N Engl J Med, 1954, 251, 1048. Lim son, B. M., Romansky, M. J., and Shea, J. G.: An evaluation of twenty-two patients with acute and chronic pulmonary infection with fried1ander's bacillus, Ann Intern Med, 1956,44, 1070. Liu, Y. K.: Leukopenia in alcoholics, Am J Med, 1973,54, 605. McFarland, W., and Libre, E. P.: Abnormal leukocyte response in alcoholism, Ann Intern Med, !963, 59, 865. Chodosh, S.: Examination of sputum cells, N Engl J Med, 1970,282,854. Pierce, A. K., and Sanford, J.P.: Aerobic gramnegative bacillary pneumonias, Am Rev Respir Dis, 1974,110, 647. Moellering, R. C., Kunz, L. J.: Determination of susceptibility of 24,108 gram-negative bacteria to tobramycin and other antibiotics utilizing a computerized system with electronic zone analyzer, Selected Proceedings, 8th International Congress of Chemotherapy, Sept 8-15, 1973, p. 72.
RICHARD J. WALLACE, JR., ROBERT J. AWE, and R. RUSSELL MARTIN 4
SUMMARY __________________________________________ ______________ A case of community-acquired pneumonia with Acinetobacter calcoacetium var. anitratus (Herellea vaginicola) is presented. Initial leukopenia and sparse leukocytes in the sputum, followed by prolonged leukocytosis and fever, were unusual features of this case. The clinical significance and current antimicrobial drug therapy of acinetobacter infections are discussed.
Introduction Bacterial pneumonia remains one of the most important complications associated with chronic alcoholism. Most of these pneumonias are pneumococcal or anaerobic in origin, but occasionally a primary aerobic gram-negative pneumonia occurs (1). These cases are often fatal, especially when associated with leukopenia. With the use of transtracheal aspiration and newer chemotherapeutic agents, more rapid diagnosis and better survival with these gram-negative pneumonias should be possible. This is the report of a case of bacteremic lobar pneumonia (Received in original form December 15, 1975 and in revised form February l!J, 1976) 1 From the Infectious Disease Division, Departments of Medicine, and Microbiology and Immunology, Baylor College of Medicine, Houston, Tex., and the Pulmonary Disease Division of Jefferson Davis Hospital, Department of Medicine, Baylor College of Medicine, Houston, Tex. 2 Supported by NIH Training Grant USPH AI00446-04 1o5. 3 Requests for reprints should be addressed to Richard J. Wallace, Jr., M.D., Department of Medicine, Baylor College of Medicine, 1200 Moursund Avenue, Houston, Tex. 77030. 4 Dr. Martin is supported by a Research Career Development Award, USPH AI 70335-02 from the National Institutes of Health.
with Acinetobacter calcoacetium var. anitratus (Herellea vaginicola), which is an aerobic, nonfermenting, gram-negative organism. Despite the presence of chronic alcoholism and leukopenia, this patient survived with appropriate antimicrobial drugs and supportive therapy. This case represents one of the few reported survivals of a community-acquired or bacteremic pneumonia with this organism. Case Report
The patient was a 50-year-old male alcoholic who was admitted to the hospital on August 1, 1975 with a 5-day history of fever, cough, and shortness of breath, and a 1-day history of confusion. The patient had been in good health most of his life, except for chronic alcohol abuse and several episodes of respiratory tract infections. He had a cumulative cigarette consumption of 30 pack-years but denied chronic sputum production or exertional dyspnea. The patient had been admitted to another hospital on May 28, 1975 for the treatment of acute diverticulitis of the colon. A chest roentgenogram at that time was interpreted as possibly showing a right lower lobe infiltrate. The leukocyte count was normal, and a sputum culture yielded normal throat flora. A 2-day course of low-dose penicillin was given. The patient then felt well until the onset of respiratory symptoms 2 months later. On admission to this hospital, the patient was an alert, but confused man in moderate respiratory distress. Vital signs included: blood pressure, 100/70 mm Hg; temperature, 100• F; pulse,
AMERICAN REVIEW OF RESPIRATORY DISEASE, VOLUME ll3, 1976
695
696
WALLACE, AWE, AND MARTIN
120 per min, and respirations, 36 per min. There was no scleral icterus. The neck was supple. There was dullness to percussion and rales over the right upper lobe. Skin turgor was poor, but there were no skin lesions or clubbing and no signs of chronic liver disease. Neurologic examination revealed a disoriented, confused man who was hallucinating, but with no focal neurologic signs. Laboratory data included hematocrit, 44 per cent; leukocyte count, 2,400 cells per mm3, with 16 per cent polymorphonuclears, 24 per cent band forms, 8 per cent metamyelocytes, and 44 per cent lymphocytes; platelet count, 30,500 per mm3; blood urea nitrogen, 24 mg per 100 ml; creatinine, 1.0 mg per 100 ml; sodium, 121 mEq per liter; potassium, 2.7 mEq per liter; chloride, 86 mEq per liter; carbon dioxide combining power, 15 mEq per liter; prothrombin time, 10.2 sec, with a control of 10.2 sec; serum glutamic oxaloacetic transaminase, 51 units; alkaline phosphatase, 96 units; bilirubin, 0.7 mg per 100 ml; calcium, 6.1 mg per 100 ml; mag-
nesium, l.l mg per 100 mi. The urinalysis showed 2plus protein and 1 to 3 white cells per high-power field. The chest radiograph showed a dense alveolar infiltrate involving anterior and posterior segments of the right upper lobe (figure 1). A transtracheal aspirate on admission yielded a moderately cellular specimen that contained 80 per cent pigmented alveolar macrophages and only 20 per cent polymorphonuclear leukocytes on wet specimen examination. Grain stain showed sheets of gramnegative cocci in singles and pairs, many of them intracellular (figure 2). Bone marrow aspiration revealed a hypocellular specimen with megakaryocytes present. There was marked vacuolization of erythroid and myeloid precursors, with virtual absence of granulocytes beyond the promyelocytic stage. No megaloblastic changes were present. Spinal fluid obtained by lumbar puncture was normal except for a total protein of 130 mg per 100 mi. Antimicrobial drug therapy was begun with 140 mg of gentamicin given intramuscularly every 8 hours (6 mg per kg
Fig. 1. Admission chest roentgenogram showing a dense right upper lobe infiltrate.
BACTEREMIC ACINETOBACTER PNEUMONIA
697
Fig. 2. Gram stain of the tracheal aspirate revealing both alveolar macrophages and polymorpho· nuclear leukocytes. Numerous gram-negative cocci in singles and pairs are present. Many of the organisms are intracellular (original magnification: X 1,000). per day), and 36 g of carbenicillin per day given intravenously. The patient required intubation because of hypoxia, with the chest radiograph showing progressive involvement of the right middle and low· er lobes. The patient's condition then stabilized on medical therapy, and slow, but gradual, improvement occurred during the next 4 weeks. Culture of tracheal aspirate and blood grew only A. calcoacetium var. anitratus (H. vaginicola); identification of both isolates was confirmed at the Texas State
Department of H ealth Laboratories. The organism was susceptible by disc to tetracycline, kanamycin, colistin, gentamicin, and carbenicillin. The minimal inhibitory concentration (MIC) for carbenicillin was 8.0 ,...g per ml; for gentamicin, 1.0 ,...g per ml. While the patient received 140 mg of gentamicin every 8 hours, serum gentamicin concentrations at I and 2 hours after a dose were 3 to 5 times the MIC for acinetobacter, whereas concentrations at 8 hours were usually still greater than the MIC (mean, 1.2
698
WALLACE, AWE, AND MARTIN
p.g per ml). The patient was treated for 2 weeks with gentamicin and carbenicillin, then received oral tetracycline for an additional week. The sputum was positive for acinetobacter on culture and Gram stain for 3 days, then became negative. The patient was leukopenic for 3 days, after which the white blood cell count increased rapidly. It peaked at 17 days at 47,000 cells per mm3 with 90 per cent polymorphonuclear leukocytes, then very slowly decreased. The leukocyte count was increased for the entire 5-week hospitalization, and was still 19,800 cells per mm3 on discharge. The platelet counts returned to normal. The patient was febrile for a total of 4.5 weeks, during which time an extensive examination for metastatic infection, tuberculosis, or carcinoma to explain the prolonged fever was negative. Bronchoscopy performed in the third week of hospitalization was normal, and right upper lobe brushings revealed no bacteria, fungi, or acid-fast organisms in smears or culture. Numerous sputum cytologic studies were negative. All cultures for tuberculosis, including cerebrospinal fluid, sputum, and bronchial washings, were negative, as were fungal serologies. The fever finally resolved without further antimicrobial drug therapy. The chest radiograph showed gradual clearing of the right middle and lower lobe infiltrates. One month after discharge, the right upper lobe infiltrate still persisted, but with significant retraction and loss of volume. At that time, the patient was asymptomatic, had gained 20 pounds since discharge, and his total leukocyte and differential counts had returned to normal. Discussion Acinetobacter are aerobic gram-negative organisms that clinically resemble the enterobacteriaceae. They differ biochemically, however, as they do not ferment carbohydrates. Both H. vaginicola and Mima polymorpha have been reclassified as acinetobacter. (For purposes of this paper, however, references to acinetobacter will refer only to A. calcoacetium var. anitratus, the new name for herellea.) Previous colonization studies have shown that as many as 25 per cent of normal persons harbor acinetobacter on their skin (2), and as many as 7 per cent carry small numbers of organisms in their throat (3). Despite this apparent ubiquity, acinetobacter has been an infrequent clinical isolate and a rare cause of community-acquired disease. Recent reviews have stressed that acinetobacter is becoming a more frequent sputum bacterial isolate, especially in the hospitalized patient who requires ventilatory support. In a recent study reporting respiratory isolates of acinetobacter, 31 of 37 patients had a tracheostomy or an endotracheal tube (4). The facts that in very few cases has the organism been isolated
on initial sputum culture (4, 5), and that acinetobacter has been isolated more frequently from hospital environmental sites than from patients (6), suggest that most isolates are nosocomially acquir~d. Clinical pneumonia has generally been restricted to severely ill patients on ventilatory support. Significant bacteremia with acinetobacter has usually been associated with indwelling venous catheter infections (7, 8) and only rarely with other conditions (9). Many blood isolates have no relationship to clinical disease, and probably represent skin contamination or insignificant bacteremia (4, 5). Only 3 of the previously reported pneumonias with acinetobacter have had associated bacteremia (10-12). There have been 4 well-documented case reports of community-acquired pneumonia with acinetobacter, 3 of which occurred in compromised hosts (10-13). Two of these patients had chronic renal disease, and one of them, like our patient, was an alcoholic. None had leukopenia. Leukopenia with bacterial pneumonias has generally been a poor prognostic sign. With pneumonia due to Streptococcus pneumoniae or klebsiella, the highest mortality has been among patients with leukopenia (14, 15). A common factor in most of these cases has been the presence of alcoholism. Recent studies have suggested that chronic alcohol consumption directly suppresses granulocyte production (16, 17). In the presence of infection, leukopenia develops as diminished granulocyte reserves become depleted. This phenomenon has been documented with infections due to both gram-positive and gram-negative organisms (17) and may be the explanation for the leukopenia in many of the previously noted pneumonias in alcoholics. This patient has the clinical course and laboratory findings of alcohol-induced marrow suppression as described by Liu (16) and McFarland (17). Like many of their cases, the leukopenia was accompanied by thrombocytopenia. The degree and duration of the rebound leukocytosis, however, was greater than that seen in any of their patients. Of interest was the initial paucity of granulocytes in the tracheal aspirate, which constituted less than 20 per cent of the cells on wet specimen examination (18). This persisted until the return of normal peripheral granulocyte counts. At that time, the sputum became purulent for the first time, with conversion to more than 90 per cent polymorphonuclear leukocytes. Antimicrobial drug therapy for severely ill pa-
BACTEREMIC ACINETOBACTER PNEUMONIA
tients with gram-negative pneumonia has usually used combination therapy (19). When Pseudomonas aeruginosa is not suspected, a popular therapeutic regimen has been cephalothin and gentamicin. With a Gram stain or a culture suggesting acinetobacter, initial therapy should probably include an aminoglycoside plus carbenicillin. Acinetobacter is resistant to the cephalosporins but is usually susceptible to carbenicillin. Unlike most enteric organisms, acinetobacter is more likely to be susceptible to kanamycin than to gentam1cm (20). Ultimate choice of antimicrobial drug therapy, as always, must depend on laboratory susceptibility tests of the specific organism. The previous fatal cases of community-acquired pneumonia with acinetobacter were either misdiagnosed or received inadequate antimicrobial drug therapy. None of them received carbenicillin or an adequate cour~e of gentamicin. Better survival in future cases may be possible with more rapid diagnosis and use of better chemotherapeutic agents. Acknowledgment
7.
8.
9.
10.
II.
12.
13.
14.
The writers acknowledge and appreciate the expert secretarial preparation of Phyllis Faulkner. References l. Tillotson, J. R., and Lerner, A. M.: Pneumonias caused by gram-negative bacilli, Medicine (Baltimore), 1966,45,65. 2. Taplin, D., Rebell, G., and Zaias, N.: The human skin as a source of mimae-herellea infections, JAMA, 1963, 186, 952. 3. Rosenthal, S., and Tager, I. B.: Prevalence of gram-negative rods in the normal pharyngeal flora, Ann Intern Med, 1975,83,355. 4. Gardner, P., Griffin, W. B., Swart, M. N., and Kunz, L. J.: Nonfermentative gram-negative bacilli of nosocomial interest, Am J Med, 1970, 48, 735. 5. Robinson, R. G., Garrison, R. G., and Brown, R. W.: Evaluation of the clinical significance of the genus herellea, Ann Intern Med, 1964, 60, 19. 6. Johanson, W. G., Jr., Pierce, A. K., Sanford, J.P., and Thomas, G. D.: Nosocomial respiratory in-
15.
16. 17.
18. 19.
20.
699
fections with gram-negative bacilli, Ann Intern Med, 1972,77, 701. Daly, A. K., Postic, B., and Kass, E. H.: Infections due to organisms of the genus herellea, Arch Intern Med, 1962,110,580. Green, G. S., Johnson, R. H., Jr., and Shively, J. A.: Mimae: Opportunistic pathogens. A review of infections in a cancer hospital, JAMA, 1966,194, 1065. King, 0. H., Copeland, G. D., and Berton, W. M.: Cardiovascular lesions of the mimae organisms, Am J Med, 1963,35,241. Wands, J. R., Mann, R. B., Jackson, D., and Butler, T.: Pneumonia in chronic renal disease, Am Rev Respir Dis, 1973, 108,964. Hammett, J. B.: Death from pneumonia with bacteremia due to mimae tribe bacterium, JAMA, 1968,206,641. Glick, L. M., Moran, G. P., Coleman, J. M., and O'Brien, G. F.: Lobar pneumonia with bacteremia caused by Bacterium anitratum, Am J Med, 1959,27,183. Gardner, D. L., Pines, A., and Stewart, S. M.: Fulminating and fatal pneumonia and septicemia due to Achromobacter anitratus, Br Med J, 1960,1' ll08. Van Metre, T. E.: Pneumococcal pneumonia treated with antibiotics: The prognostic significance of certain clinical findings, N Engl J Med, 1954, 251, 1048. Lim son, B. M., Romansky, M. J., and Shea, J. G.: An evaluation of twenty-two patients with acute and chronic pulmonary infection with fried1ander's bacillus, Ann Intern Med, 1956,44, 1070. Liu, Y. K.: Leukopenia in alcoholics, Am J Med, 1973,54, 605. McFarland, W., and Libre, E. P.: Abnormal leukocyte response in alcoholism, Ann Intern Med, !963, 59, 865. Chodosh, S.: Examination of sputum cells, N Engl J Med, 1970,282,854. Pierce, A. K., and Sanford, J.P.: Aerobic gramnegative bacillary pneumonias, Am Rev Respir Dis, 1974,110, 647. Moellering, R. C., Kunz, L. J.: Determination of susceptibility of 24,108 gram-negative bacteria to tobramycin and other antibiotics utilizing a computerized system with electronic zone analyzer, Selected Proceedings, 8th International Congress of Chemotherapy, Sept 8-15, 1973, p. 72.
