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Chlamydia pneumoniae infections

Kalayoglu, M.V., Byrne, G.I., 1998b, Induction of macrophage foam ceU formation by Chlamydia pneumoniae,/. Infect. Dis. 177 725-729. [Pg.145]

Siiram S, Stratton CW, Yao S, Tharp A, Duig L, Bannan ID, Mitchell WM (1999) Chlamydia pneumoniae infection of the central nervous system in multiple sclerosis. Ann Neurol 46 6—14. [Pg.256]

Anderson JL, Muhlestein JB, Carlquist J, Allen A, Trehan S, Nielson C, Hall S, Brady J, Egger M, Horne B, Lim T. Randomized secondary prevention trial of azithromycin in patients with coronary artery disease and serological evidence for Chlamydia pneumoniae infection The Azithromycin in Coronary Artery Disease Elimination of Myocardial Infection with Chlamydia (ACADEMIC) study. Circulation 1999 99(12) 1540-7. [Pg.2190]

Geng Y, Berencsi K, Gyulai Z, Valyi-Nagy T, Gonczol E, Trinchieii G. Roles of interleukin-12 and gamma interferon in murine Chlamydia pneumoniae infection. Infect Immiin 2000 68(4) 2245-2253. [Pg.211]

The major precipitants of exacerbations of COPD are acute airways infections. The role of bacteria in precipitating exacerbations is controversial. Bacteria may have a primary role in the development of an exacerbation or represent a secondary superinfection of an initial viral process. The major bacterial organisms that have been associated with exacerbations are Haemophilus influenzae. Streptococcus pneumoniae, and Moraxella (Branhamella) catarrhalis. Mycoplasma pneumoniae and Chlamydia pneumoniae may play a part. In COPD patients with a FEVi < 35% predicted gram-negative bacteria, especially Enterobacteriaceae and Pseudomonas spp. play an important part in acute exacerbations. [Pg.646]

Kalayoglu, M.V., and Byrne, G.I., 1998a, A Chlamydia pneumoniae component that induces macrophage foam cell formation is chlamydial hpopolysaccharide, Infect. Immun. 66 5067-5072. [Pg.145]

Due to its powerful specific activity against commonly isolated community-acquired respiratory tract pathogens [33,149-158], including penicillin-sensitive and -resistant Streptococcus pneumoniae, methicillin-sensitive Staphylococcus aureus, Haemophilus spp., Moraxella catarrhalis and atypical pathogens such as Mycoplasma pneumoniae, Chlamydia pneumoniae and Legionella pneumophila and Klebsiella pneumoniae and anaerobic bacteria [159-162], moxifloxacin was developed as a respiratory tract anti-infective [163-168]. [Pg.344]

Yersinia and Camplyobacter, as well as chronic Lyme arthritis. Human studies are currently underway to investigate a possible link between coronary artery disease and infection with Chlamydia pneumoniae. [Pg.242]

Kornak.J., Kuo, C., and Campbell, L. (1991). Sequence analysis of the gene encoding the Chlamydia pneumoniae DnaK protein homolog. Infect. Immun. 59, Ti —T2.b. [Pg.95]

Maaolides are appropriate antibiotics for the management of respiratory tract infections because they are active against Streptococcus pneumoniae. Streptococcus pyogenes (group A streptococci), and atypical organisms such as Legionella pneumophila. Mycoplasma pneumoniae, and Chlamydia pneumoniae. The newer generation macrolides such as clar-... [Pg.113]

Falck G, Gnarpe J, Gnarpe H. Prevalence of Chlamydia pneumoniae in healthy children and in children with respiratory tract infections. Pediatr Infect Dis J 1997 16 549-554. [Pg.1960]

Eile TM, Tan JS, Plouffe JE. The role of atypical pathogens Mycoplasma pneumoniae, Chlamydia pneumoniae and Legionella pneumophila in respiratory infection. Infect Dis Clin North Am 1998 12 569-592. [Pg.1961]

Inflammation of blood vessel walls induces cellular proliferation, oxidation and deposition of cholesterol, and the development of atherosclerosis. These are ideal culture conditions for some tough bacteria, such as Chlamydia pneumoniae, which infect damaged arterial walls, and from their safe haven antagonize immune cells. Up to 80 per cent of people with cardiovascular disease are infected with Chlamydia, but whether this is a cause or an effect of heart disease is still disputed. It is simplest to say it could be both the cause of atherosclerosis is oxidative stress, and the process can be started, or perpetuated, by smoking, AGEs, oxidized cholesterol, ApoE4, infections, or just old age. Any one of these factors makes the others more likely. All are united by oxidative stress, and converted into the common currency of inflammation by NFkB and its kin. [Pg.311]

Yaraei, K, Campbell, L A, Zhu, X, Liles, W C, Kuo, C C, and Rosenfeld, M E, Chlamydia pneumoniae Augments the oxidized low-density lipoprotein-induced death of mouse macrophages by a caspase-independent pathway. Infect. Immun. 73 (2005) 4315-4322. [Pg.369]


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