Angaben zur Quelle [Bearbeiten]
| Autor | S. Sethi |
| Titel | Infection as a comorbidity of COPD |
| Zeitschrift | European Respiratory journal |
| Ausgabe | 35 |
| Jahr | 2010 |
| Nummer | 6 |
| Seiten | 1209-1215 |
| ISSN | 1399-3003 |
| DOI | 10.1183/09031936.00081409 |
| URL | http://erj.ersjournals.com/content/35/6/1209.full.pdf |
Literaturverz. |
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| Fußnoten | yes |
| Fragmente | 1 |
| [1.] Analyse:Amm/Fragment 023 07 - Diskussion Zuletzt bearbeitet: 2014-12-25 21:05:26 Hindemith | Amm, Fragment, KomplettPlagiat, SMWFragment, Schutzlevel, Sethi 2010, ZuSichten |
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| Untersuchte Arbeit: Seite: 23, Zeilen: 7-29 |
Quelle: Sethi 2010 Seite(n): 1210, Zeilen: l.col: 18ff |
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| Early studies based on culture of respiratory secretions and serological tests revealed that about one-third of exacerbations were related to bacterial infection. However, in the remaining cases, the aetiology appeared to be uncertain; specifically, the significance of bacterial isolation from sputum was unclear (Gump DW et al, 1976). A causal relationship between bacteria and exacerbation was largely discredited when longitudinal studies showed similar rates of isolation of Streptococcus pneumoniae and Haemophilus influenzae from sputum during both acute exacerbations and stable disease (Fagon JY et al, 1996; Gump DW et al, 1976; McHardy VU et al, 1980; Smith CB et al, 1976; Tager I et al, 1975). A significant limitation of these studies was their failure to differentiate among strains within a bacterial species (Sethi S et al, 2002), as the technology was not available at that time for such differentiation. Consequently, changes in strains within a species in the airways of individual patients over time were undetected.
In recent years, new research techniques, including molecular typing, have led to renewed interest in the area of bacteria and COPD. Recent studies have used more sophisticated diagnostic tools and the application of molecular technologies to further explore a causal relationship between infection and exacerbation. Acquisition of new bacterial strains from the environment has been shown to be the major driver of exacerbations (Veeramachaneni SB et al, 2006). In this model, following acquisition of a new bacterial strain, the balance between the virulence of the pathogen and the host lung defence determines the degree of excess airway and systemic inflammation engendered by the bacterial pathogen. The degree of increased inflammation in turn determines the extent of symptoms, which, if they lead to the patient seeking [healthcare, are diagnosed as an acute exacerbation.] |
Early studies based on culture of respiratory secretions and serological tests revealed that about one-third of exacerbations were related to viral infection. However, in the remaining cases, the aetiology appeared to be uncertain; specifically, the significance of bacterial isolation from sputum was unclear [4]. A causal relationship between bacteria and exacerbation was largely discredited when longitudinal studies showed similar rates of isolation of Streptococcus pneumoniae and Haemophilus influenzae from sputum during both acute exacerbations and stable disease [4–8]. A significant limitation of these studies was their failure to differentiate among strains within a bacterial species [9], as the technology was not available at that time for such differentiation. Consequently, changes in strains within a species in the airways of individual patients over time were undetected.
In recent years, new research techniques, including molecular typing, have led to renewed interest in the area of bacteria and COPD. Recent studies have used more sophisticated diagnostic tools and the application of molecular technologies to further explore a causal relationship between infection and exacerbation. [...] An alternative model that is now well supported with empirical evidence is based on the premise that acquisition of new bacterial strains from the environment is the major driver of exacerbations (fig. 2) [12]. In this model, following acquisition of a new bacterial strain, the balance between the virulence of the pathogen and the host lung defence determines the degree of excess airway and systemic inflammation engendered by the bacterial pathogen. The degree of increased inflammation in turn determines the extent of symptoms, which, if they lead to the patient seeking healthcare, are diagnosed as an acute exacerbation. 4 Gump DW, Phillips CA, Forsyth BR, et al. Role of infection in chronic bronchitis. Am Rev Respir Dis 1976; 113: 465–474. 5 McHardy VU, Inglis JM, Calder MA, et al. A study of infective and other factors in exacerbations of chronic bronchitis. Br J Dis Chest 1980; 74: 228–238. 6 Smith CB, Golden C, Klauber MR, et al. Interactions between viruses and bacteria in patients with chronic bronchitis. J Infect Dis 1976; 134: 552–561. 7 Fagon JY, Chastre J. Severe exacerbations of COPD patients: the role of pulmonary infections. Semin Respir Infect 1996; 11: 109–118. 8 Tager I, Speizer FE. Role of infection in chronic bronchitis. N Engl J Med 1975; 292: 563–571. 9 Sethi S, Evans N, Grant BJ, et al. New strains of bacteria and exacerbations of chronic obstructive pulmonary disease. N Engl J Med 2002; 347: 465–471. 12 Veeramachaneni SB, Sethi S. Pathogenesis of bacterial exacerbations of COPD. COPD 2006; 3: 109–115. |
The source is not mentioned here. Note that in the first sentence "viral" was changed to "bacterial". From the abstract of the original source Gump et al. (1976): "One third (33.6 per cent) of the 116 exacerbations observed could be related to viral infection or Mycoplasma pneumoniae (1 exacerbation)." |
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