Legionella Pneumonia

Kazuhiro Tateda

doi:10.20965/jdr.2011.p0435

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JDR Vol.6 No.4 pp. 435-442

(2011)

doi: 10.20965/jdr.2011.p0435

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Legionella Pneumonia

Kazuhiro Tateda

Department of Microbiology and Infectious Diseases, Toho University School of Medicine, 5-21-16 Ohmorinishi, Ohtaku, Tokyo 143-8540, Japan

Received:

February 22, 2011

Accepted:

July 6, 2011

Published:

August 1, 2011

Keywords:

Legionella, pneumonia, pontiac fever, macrolide, quinolone, apoptosis

Abstract

Legionella pneumonia, an infectious disease with high fatality, produces symptoms after inhalation of an aerosol contaminated by Legionella species. Legionella bacteria are Gram-negative, glucose-nonfermentative, and proliferative in human macrophages and monocytes. Over 40 types of Legionella species are pathogenic in human beings. Of these, L. pneumophila has the strongest pathogenicity. Hot springs and bathtubs with circulating systems are considered sources of infection and sometimes cause cases of hospital-acquired infection. The urinary antigen detection test is a new diagnostic technique, and proved to be effective for rapid and correct diagnosis of L. pneumophila serogroup-1 infection.

Cite this article as:

K. Tateda, “Legionella Pneumonia,” J. Disaster Res., Vol.6 No.4, pp. 435-442, 2011.

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References

[1] B. J. Marston, H. B. Lipman, and R. F. Breiman, “Surveillance for Legionnaires’ desease. Risk factors for morbidity and mortality,” Arch. Intern. Med., Vol.154, pp. 2417-2422, 1994.
[2] R. Bohte, R. von Furth, and P. J. van den Broek, “Aetiology of community-acquired pneumonia: a prospective study among adults requiring admission to hospital,” Thorax, Vol.50, pp. 543-547, 1995.
[3] D. Lieberman, A. Porath, F. Schlaeffer, D. Lieberman, and I. Boldur, “Legionella species community-acquired pneumonia. A review of 56 hospitalized adult patients,” Chest, Vol.109, pp. 1243-1249, 1996.
[4] A. L. Benin, R. F. Benson, and R. E. Besser, “Trends in Legionnaires disease, 1980-1998: declining mortality and new patterns of diagnosis,” Clin Infect Dis, Vol.35, pp. 1039-1046, 2002.
[5] A. Saito, T. Shimoda, M. Nagasawa, H. Tanaka, N. Ito, Y. Shigeno, K. Yamaguchi, M. Hirota, M. Nakatomi, and K. Hara, “The first case of Legionnaires’ disease in Japan,” the Journal of Japanese Association for Infectious Diseases, Vol.55, pp. 124-128, 1981 (in Japanese).
[6] Infectious Disease Surveillance Center,
http://idsc.nih.go.jp/idwr/index.html
[7] K. Neil and R. Berkelman, “Increasing incidence of legionellosis in the United States, 1990-2005: changing epidemiologic trends,” Clin Infect Dis, Vol.47, pp. 591-599, 2008.
[8] “Prevention Guidelines against Legionnaires’ Disease (3rd Edition),” Foundation Building Management Education Center, Mar. 2009 (in Japanese).
[9] C. H. Mody, R. Paine 3rd, M. S. Shahrabadi, et al., “Legionella pneumophila replicates within rat alveolar epithelial cells,” J. Infect. Dis., Vol.167, p. 1138, 1993.
[10] K. Tateda, T. Matsumoto, Y. Ishii, et al., “Serum cytokines in patients with Legionella pneumonia: relative predominance of Th1-type cytokines,” Clin Diagn Lab Immunol, Vol.5, p. 401, 1998.
[11] J. C. Deng, K. Tateda, X. Zeng, et al., “Transient transgenic expression of gamma interferon promotes Legionella pneumophila clearance in immunocompetent hosts,” Infect Immun, Vol.69, pp. 6382-6390, 2001.
[12] K. Tateda, T. A. Moore, J. C. Deng, et al., “Early recruitment of neutrophils determines subsequent T1/T2 host responses in a murine model of Legionella pneumophila pneumonia,” J Immunol, Vol.166, pp. 3355-3361, 2001.
[13] L. Y. Gao and Y. Abu Kwaik, “Apoptosis in macrophages and alveolar epithelial cells during early stages of infection by Legionella pneumophila and its role in cytopathogenicity,” Infect Immun, Vol.67, pp. 862-870, 1999.
[14] K. Tateda, J. C. Deng, T. A. Moore, et al., “Hyperoxia mediates acute lung injury and increased lethality in murine Legionella pneumonia: the role of apoptosis,” J Immunol., Vol.170, pp. 4209-4216, 2003.
[15] F. Sakai, H. Tokuda, H. Goto, K. Tateda, T. Johkoh, H. Nakamura, T. Matsuoka, A. Fujita, Y. Nakamori, S. Aoki, and S. Ohdama, Computed tomographic features of Legionella pneumophila pneumonia in 38 cases, J Comput Assist Tomogr, Vol.31, pp. 125-131, 2007.

This article is published under a Creative Commons Attribution-NoDerivatives 4.0 Internationa License.

[1] [1] B. J. Marston, H. B. Lipman, and R. F. Breiman, “Surveillance for Legionnaires’ desease. Risk factors for morbidity and mortality,” Arch. Intern. Med., Vol.154, pp. 2417-2422, 1994.

[2] [2] R. Bohte, R. von Furth, and P. J. van den Broek, “Aetiology of community-acquired pneumonia: a prospective study among adults requiring admission to hospital,” Thorax, Vol.50, pp. 543-547, 1995.

[3] [3] D. Lieberman, A. Porath, F. Schlaeffer, D. Lieberman, and I. Boldur, “Legionella species community-acquired pneumonia. A review of 56 hospitalized adult patients,” Chest, Vol.109, pp. 1243-1249, 1996.

[4] [4] A. L. Benin, R. F. Benson, and R. E. Besser, “Trends in Legionnaires disease, 1980-1998: declining mortality and new patterns of diagnosis,” Clin Infect Dis, Vol.35, pp. 1039-1046, 2002.

[5] [5] A. Saito, T. Shimoda, M. Nagasawa, H. Tanaka, N. Ito, Y. Shigeno, K. Yamaguchi, M. Hirota, M. Nakatomi, and K. Hara, “The first case of Legionnaires’ disease in Japan,” the Journal of Japanese Association for Infectious Diseases, Vol.55, pp. 124-128, 1981 (in Japanese).

[6] [6] Infectious Disease Surveillance Center,
http://idsc.nih.go.jp/idwr/index.html

[7] [7] K. Neil and R. Berkelman, “Increasing incidence of legionellosis in the United States, 1990-2005: changing epidemiologic trends,” Clin Infect Dis, Vol.47, pp. 591-599, 2008.

[8] [8] “Prevention Guidelines against Legionnaires’ Disease (3rd Edition),” Foundation Building Management Education Center, Mar. 2009 (in Japanese).

[9] [9] C. H. Mody, R. Paine 3rd, M. S. Shahrabadi, et al., “Legionella pneumophila replicates within rat alveolar epithelial cells,” J. Infect. Dis., Vol.167, p. 1138, 1993.

[10] [10] K. Tateda, T. Matsumoto, Y. Ishii, et al., “Serum cytokines in patients with Legionella pneumonia: relative predominance of Th1-type cytokines,” Clin Diagn Lab Immunol, Vol.5, p. 401, 1998.

[11] [11] J. C. Deng, K. Tateda, X. Zeng, et al., “Transient transgenic expression of gamma interferon promotes Legionella pneumophila clearance in immunocompetent hosts,” Infect Immun, Vol.69, pp. 6382-6390, 2001.

[12] [12] K. Tateda, T. A. Moore, J. C. Deng, et al., “Early recruitment of neutrophils determines subsequent T1/T2 host responses in a murine model of Legionella pneumophila pneumonia,” J Immunol, Vol.166, pp. 3355-3361, 2001.

[13] [13] L. Y. Gao and Y. Abu Kwaik, “Apoptosis in macrophages and alveolar epithelial cells during early stages of infection by Legionella pneumophila and its role in cytopathogenicity,” Infect Immun, Vol.67, pp. 862-870, 1999.

[14] [14] K. Tateda, J. C. Deng, T. A. Moore, et al., “Hyperoxia mediates acute lung injury and increased lethality in murine Legionella pneumonia: the role of apoptosis,” J Immunol., Vol.170, pp. 4209-4216, 2003.

[15] [15] F. Sakai, H. Tokuda, H. Goto, K. Tateda, T. Johkoh, H. Nakamura, T. Matsuoka, A. Fujita, Y. Nakamori, S. Aoki, and S. Ohdama, Computed tomographic features of Legionella pneumophila pneumonia in 38 cases, J Comput Assist Tomogr, Vol.31, pp. 125-131, 2007.