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Bacteremic Moraxella catarrhalis pneumonia in a patient with immunoglobulin deficiency
J Infect Chemother (2000) 6:61–62
© Japan Society of Chemotherapy 2000
CASE REPORT Hajime Sugiyama · Eri Ogata · Yuko Shimamoto Youji Koshibu · Kaoru Matsumoto · Keiko Murai Taku Miyashita · Yasuo Ono · Hajime Nishiya Otohiko Kunii · Tomohide Sato
Bacteremic Moraxella catarrhalis pneumonia in a patient with immunoglobulin deficiency
Received: May 19, 1999 / Accepted: October 8, 1999
Abstract A-75-year old woman with agammaglobulinemia developed Moraxella catarrhalis bacteremic pneumonia. M. catarrhalis pneumonia is rarely associated with bacteremia, and neutrophils have been reported as a significant factor in the host defense system against this bacteria. This case suggests that immunoglobulin also plays a key role in the host defense system against M. catarrhalis. Key words Moraxella catarrhalis · Immunoglobulin · Common variable immunodeficiency
Introduction Moraxella catarrhalis is an important pathogen that causes lower respiratory tract infection in healthy hosts and patients with chronic lung disease.1,2 Bacteremia complicating M. catarrhalis pneumonia is rare, especially in adults.1–3 We report a case of M. catarrhalis bacteremic pneumonia in a patient with agammaglobulinemia.
Case report A-75-year old woman presented to our hospital emergency room with fever, cough, purulent sputum, and anorexia in December 1996 (Fig. 1). She had been hospitalized for Staphylococcus aureus pneumonia 5 years previously. On physical examination, her temperature was 38.6°C; pulse, 106/min; and blood pressure, 112/74 mmHg. Moist rales were audible over both lungs. A chest radiograph revealed
H. Sugiyama (*) · E. Ogata · Y. Shimamoto · Y. Koshibu · K. Matsumoto · K. Murai · T. Miyashita · Y. Ono · H. Nishiya · O. Kunii · T. Sato Department of Internal Medicine, Teikyo University School of Medicine, 2-11-1 Kaga, Itabashi-ku, Tokyo 173-0003, Japan Tel./Fax 181-3-3964-2194 e-mail: [email protected]
infiltrates in the right upper and middle lung fields. Arterial blood gas values while the patient was breathing room air were: PO2, 37.7 mmHg, PCO2, 45.0 mmHg, and pH, 7.464. The white blood cell count was 40.0 3 109/l, with 15% band forms, 76% neutrophils, and 4% lymphocytes. The erythrocyte sedimentation rate was 12 mm/h, and C-reactive protein level was 23.3 mg/dl. Although concentrations of complement components were normal, immunoglobulins of all types were not detectable. The peripheral lymphocyte population was normal, including B cells, and IgM and IgD were expressed normally on B lymphocytes. In the bone marrow, lymphocytes but no plasma cells were identified. We obtained evidence of hypogammaglobulinemia (IgG, 329 mg/dl) from her medical record of hospital admission for S. aureus pneumonia 5 years previously. We diagnosed the patient with common variable immunodeficiency, in view of chronic hypogammaglobulinemia with normal lymphocyte counts and recurrent bacterial infections of the lower respiratory tract. After admission, she received imipenem, 1.5 g, given intravenously daily, in addition to oxygen therapy and intravenous immunoglobulin. Blood cultures obtained at admission yielded growth of M. catarrhalis, which was susceptible to imipenem. Sputum culture was also positive for M. catarrhalis 21, as well as Pseudomonas aeruginosa 11, which was also susceptible to imipenem. She showed a response to the initial antibiotic therapy, but her condition then worsened, and sputum culture was positive for methicillin-resistant S. aureus. On the ninth hospital day, we added vancomycin, 1.0 g, given intravenously daily, and replacement therapy for agammaglobulinemia to the patient’s initial antibiotic therapy. As P. aeruginosa obtained from her sputum on the ninth hospital day was susceptible to amikacin and imipenem, amikacin, 200 mg daily, was instituted on the 14th hospital day, in addition to the other agents. However, her condition continued to decline. She failed to recover from the pneumonia, and died of respiratory failure on the 23rd hospital day. An autopsy was performed 9.5 h after death. Postmortem microbiological tests were not performed. Gross examination of internal organs revealed multiple lung abscesses of varying age, indicative of recurrent lower respiratory
62 Fig. 1. Clinical course of a 75year-old woman with bacteremic Moraxella catarrhalis pneumonia. IPM/CS, Imipenem cilastatin; VCM, vancomycin; AMK, amikacin; γGlb, gammaglobulin; d, day; WBC, white blood cells; CRP, C-reactive protein; MRSA, methicillin-resistant Staphylococcus aureus
tract infections. All lymphoid tissues, including liver and spleen, were atrophic. We did not detect thymoma, which is associated with hypogammaglobulinemia in elderly people. Microscopically, the bone marrow showed normal cellularity and no leukemic change. No germinal centers were seen in lymph node follicles. We failed to find any mature plasma cells in any tissue, using an antibody against human plasma cells.
Discussion M. catarrhalis, while a major pathogen of the lower respiratory tract, rarely causes bacteremia.1,2 In a report of 58 cases of M. catarrhalis bacteremia, neutropenia was the leading underlying disorder.4 Neutrophils are considered to be important in the host defense against M. catarrhalis.4 Dysgammaglobulinemia underlying severe M. catarrhalis pneumonia has also been reported previously.5–7 Most patients with pulmonary infections caused by M. catarrhalis develop a convalescent IgG antibody response that mediates serum bactericidal activity.8 A monoclonal antibody specific for the surface antigen of the bacteria has been shown to promote pulmonary clearance of the organism in mice.9 Therefore, immunoglobulins may participate significantly in the host defense against M. catarrhalis. Although the influence of co-infecting pathogens could not be excluded in the present patient, this case suggests
that immunoglobulin and specific antibodies against M. catarrhalis are important for the host defenses against this organism.
References 1. Catlin BW. Branhamella catarrhalis: an organism gaining respect as a pathogen. Clin Microbiol Rev 1990;3:293–320. 2. Wright PW, Wallace RJ, Shepherd JR. A descriptive study of 42 cases of Branhamella catarrhalis pneumonia. Am J Med 1990; 88 (Suppl 5A):S2–7. 3. Enright MC, McKenzie H. Moraxella (Branhamella) catarrhalis – clinical and molecular aspects of a rediscovered pathogen. J Med Microbiol 1997;46:360–71. 4. Ioannidis JPA, Worthington M, Griffiths JK, Snydman DR. Spectrum and significance of bacteremia due to Moraxella catarrhalis. Clin Infect Dis 1995;21:390–7. 5. Cox PM, Colloff E. Neisseria catarrhalis empyema in an immunodeficient host. Am Rev Respir Dis 1979;120:471–2. 6. Diamond LA, Lorber B. Branhamella catarrhalis pneumonia and immunoglobulin abnormalities: a new association. Am Rev Respir Dis 1984;129:876–8. 7. Karnad A, Alvarez S, Berk SL. Branhamella catarrhalis pneumonia in patients with immunoglobulin abnormalities. South Med J 1986;79:1360–2. 8. Chapman AJ, Musher DM, Jonsson S, Clarridge JE, Wallace RJ. Development of bactericidal antibody during Branhamella catarrhalis infection. J Infect Dis 1985;151:878–82. 9. Helminen ME, Maciver I, Latimer JL, K-Tait J, Cope LD, Paris M, et al. A large, antigenically conserved protein on the surface of Moraxella catarrhalis is a target for protective antibodies. J Infect Dis 1994;170:867–72.
© Japan Society of Chemotherapy 2000
CASE REPORT Hajime Sugiyama · Eri Ogata · Yuko Shimamoto Youji Koshibu · Kaoru Matsumoto · Keiko Murai Taku Miyashita · Yasuo Ono · Hajime Nishiya Otohiko Kunii · Tomohide Sato
Bacteremic Moraxella catarrhalis pneumonia in a patient with immunoglobulin deficiency
Received: May 19, 1999 / Accepted: October 8, 1999
Abstract A-75-year old woman with agammaglobulinemia developed Moraxella catarrhalis bacteremic pneumonia. M. catarrhalis pneumonia is rarely associated with bacteremia, and neutrophils have been reported as a significant factor in the host defense system against this bacteria. This case suggests that immunoglobulin also plays a key role in the host defense system against M. catarrhalis. Key words Moraxella catarrhalis · Immunoglobulin · Common variable immunodeficiency
Introduction Moraxella catarrhalis is an important pathogen that causes lower respiratory tract infection in healthy hosts and patients with chronic lung disease.1,2 Bacteremia complicating M. catarrhalis pneumonia is rare, especially in adults.1–3 We report a case of M. catarrhalis bacteremic pneumonia in a patient with agammaglobulinemia.
Case report A-75-year old woman presented to our hospital emergency room with fever, cough, purulent sputum, and anorexia in December 1996 (Fig. 1). She had been hospitalized for Staphylococcus aureus pneumonia 5 years previously. On physical examination, her temperature was 38.6°C; pulse, 106/min; and blood pressure, 112/74 mmHg. Moist rales were audible over both lungs. A chest radiograph revealed
H. Sugiyama (*) · E. Ogata · Y. Shimamoto · Y. Koshibu · K. Matsumoto · K. Murai · T. Miyashita · Y. Ono · H. Nishiya · O. Kunii · T. Sato Department of Internal Medicine, Teikyo University School of Medicine, 2-11-1 Kaga, Itabashi-ku, Tokyo 173-0003, Japan Tel./Fax 181-3-3964-2194 e-mail: [email protected]
infiltrates in the right upper and middle lung fields. Arterial blood gas values while the patient was breathing room air were: PO2, 37.7 mmHg, PCO2, 45.0 mmHg, and pH, 7.464. The white blood cell count was 40.0 3 109/l, with 15% band forms, 76% neutrophils, and 4% lymphocytes. The erythrocyte sedimentation rate was 12 mm/h, and C-reactive protein level was 23.3 mg/dl. Although concentrations of complement components were normal, immunoglobulins of all types were not detectable. The peripheral lymphocyte population was normal, including B cells, and IgM and IgD were expressed normally on B lymphocytes. In the bone marrow, lymphocytes but no plasma cells were identified. We obtained evidence of hypogammaglobulinemia (IgG, 329 mg/dl) from her medical record of hospital admission for S. aureus pneumonia 5 years previously. We diagnosed the patient with common variable immunodeficiency, in view of chronic hypogammaglobulinemia with normal lymphocyte counts and recurrent bacterial infections of the lower respiratory tract. After admission, she received imipenem, 1.5 g, given intravenously daily, in addition to oxygen therapy and intravenous immunoglobulin. Blood cultures obtained at admission yielded growth of M. catarrhalis, which was susceptible to imipenem. Sputum culture was also positive for M. catarrhalis 21, as well as Pseudomonas aeruginosa 11, which was also susceptible to imipenem. She showed a response to the initial antibiotic therapy, but her condition then worsened, and sputum culture was positive for methicillin-resistant S. aureus. On the ninth hospital day, we added vancomycin, 1.0 g, given intravenously daily, and replacement therapy for agammaglobulinemia to the patient’s initial antibiotic therapy. As P. aeruginosa obtained from her sputum on the ninth hospital day was susceptible to amikacin and imipenem, amikacin, 200 mg daily, was instituted on the 14th hospital day, in addition to the other agents. However, her condition continued to decline. She failed to recover from the pneumonia, and died of respiratory failure on the 23rd hospital day. An autopsy was performed 9.5 h after death. Postmortem microbiological tests were not performed. Gross examination of internal organs revealed multiple lung abscesses of varying age, indicative of recurrent lower respiratory
62 Fig. 1. Clinical course of a 75year-old woman with bacteremic Moraxella catarrhalis pneumonia. IPM/CS, Imipenem cilastatin; VCM, vancomycin; AMK, amikacin; γGlb, gammaglobulin; d, day; WBC, white blood cells; CRP, C-reactive protein; MRSA, methicillin-resistant Staphylococcus aureus
tract infections. All lymphoid tissues, including liver and spleen, were atrophic. We did not detect thymoma, which is associated with hypogammaglobulinemia in elderly people. Microscopically, the bone marrow showed normal cellularity and no leukemic change. No germinal centers were seen in lymph node follicles. We failed to find any mature plasma cells in any tissue, using an antibody against human plasma cells.
Discussion M. catarrhalis, while a major pathogen of the lower respiratory tract, rarely causes bacteremia.1,2 In a report of 58 cases of M. catarrhalis bacteremia, neutropenia was the leading underlying disorder.4 Neutrophils are considered to be important in the host defense against M. catarrhalis.4 Dysgammaglobulinemia underlying severe M. catarrhalis pneumonia has also been reported previously.5–7 Most patients with pulmonary infections caused by M. catarrhalis develop a convalescent IgG antibody response that mediates serum bactericidal activity.8 A monoclonal antibody specific for the surface antigen of the bacteria has been shown to promote pulmonary clearance of the organism in mice.9 Therefore, immunoglobulins may participate significantly in the host defense against M. catarrhalis. Although the influence of co-infecting pathogens could not be excluded in the present patient, this case suggests
that immunoglobulin and specific antibodies against M. catarrhalis are important for the host defenses against this organism.
References 1. Catlin BW. Branhamella catarrhalis: an organism gaining respect as a pathogen. Clin Microbiol Rev 1990;3:293–320. 2. Wright PW, Wallace RJ, Shepherd JR. A descriptive study of 42 cases of Branhamella catarrhalis pneumonia. Am J Med 1990; 88 (Suppl 5A):S2–7. 3. Enright MC, McKenzie H. Moraxella (Branhamella) catarrhalis – clinical and molecular aspects of a rediscovered pathogen. J Med Microbiol 1997;46:360–71. 4. Ioannidis JPA, Worthington M, Griffiths JK, Snydman DR. Spectrum and significance of bacteremia due to Moraxella catarrhalis. Clin Infect Dis 1995;21:390–7. 5. Cox PM, Colloff E. Neisseria catarrhalis empyema in an immunodeficient host. Am Rev Respir Dis 1979;120:471–2. 6. Diamond LA, Lorber B. Branhamella catarrhalis pneumonia and immunoglobulin abnormalities: a new association. Am Rev Respir Dis 1984;129:876–8. 7. Karnad A, Alvarez S, Berk SL. Branhamella catarrhalis pneumonia in patients with immunoglobulin abnormalities. South Med J 1986;79:1360–2. 8. Chapman AJ, Musher DM, Jonsson S, Clarridge JE, Wallace RJ. Development of bactericidal antibody during Branhamella catarrhalis infection. J Infect Dis 1985;151:878–82. 9. Helminen ME, Maciver I, Latimer JL, K-Tait J, Cope LD, Paris M, et al. A large, antigenically conserved protein on the surface of Moraxella catarrhalis is a target for protective antibodies. J Infect Dis 1994;170:867–72.