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Ventilator-Associated Pneumonia in Institutionalized Elders

November 28, 2004

Are Teeth a Reservoir For Respiratory Pathogens?

Pneumonia and influenza are currently the seventh leading cause of death in the United States, with approximately 65,984 deaths occurring in 2002, for an overall death rate of 22.9 per 100,000 population.1 In the elderly, defined as age ≥ 65 years, pneumonia and influenza are the fifth leading cause of death, with 59,235 deaths and an overall death rate of 166.4 per 100,000. In other words, approximately 90% of deaths related to this disease combination occur at ≥ 65 years of age. More than 98% of these deaths are secondary to pneumonia, with a minor contribution from influenza.

Hospital-acquired pneumonia, a pneumonia subtype defined as occurring ≥ 48 to 72 h after admission to the hospital, can he divided into ventilator-associated pneumonia (VAP) and nonventilator- associated types. It occurs in anywhere from 0.5 to 5% of hospitalized patients,2 and is the second most common hospital- acquired infection in elderly patients after the urinary tract. It is the leading cause of death from nosocomial infections, with an approximate mortality of 16% in the elderly population.3 Nosocomial pneumonia narrowed down to VAP, defined as pneumonia developing at least 48 h after intubation, has an even higher mortality, varying from 17 to at least 50%,4,5 with an attributable cost when matched to other ventilator patients without pneumonia of $11,897 per event.5 Given an aging population and the expense that will only climb with improved technology, understanding the pathophysiology of this type of pneumonia for prevention purposes will help to markedly reduce cost and improve health outcomes.

Currently it is believed that bacterial colonixation of the upper respiratory tract, including the normally sterile trachea and endotracheal tube in intubated patients, is a precursor to aspiration of organisms into the distal lung with the subsequent occurrence of VAP. As the severity of illness increases and the time in a critical care environment adds up the degree of colonization with respiratory pathogens, including Staphylococcus aureus, Streptococcus pneumoniae, and Gram-negative rods (especially Haemophilus influenzae, Enterobacteriaceae, Pseudomonas aeruginosa, and Acinetobacter baumanii) increases to > 70%.6-8 Many studies8-10 have revealed similar organisms in the distal airway of pneumonia patients and the trachea and oropharynx. In particular, one study11 compared the chromosomal DNA pattern of oropharyngeal samples in patients receiving mechanical ventilation prior to the development of VAP and bronchoscopically derived samples after the development of VAP, and found identical genetic matches in 17 of 18 cases in those with acquired pneumonia. This study validates the predominant theory that most but not all cases of VAP are probably secondary to colonization of the trachea or oropharynx with subsequent aspiration, defined as exogenous bacterial colonization. Some bacteria, such as the Enterobacteriaceae, can either reflux from the GI tract (endogenous colonization), colonize the upper airway or trachea, and then develop a subsequent aspiration or start in the trachea or oropharynx and aspirate; both occurred in this study.11 However, the predominant mode of distal lung infection is believed to be exogenous, as occurred in this study.11

Two studies12,13 in ICU patients have suggested that dental plaque can harbor respiratory pathogens. The first study12 found respiratory pathogens present in both dental plaque (18 of 20 with teeth) and buccal mucosa (24 of 34 with and without teeth) in 34 ICU patients in contrast to only 4 of 25 dental patients of similar age. In a second study13 of 57 ICU patients (44 of 57 intubated) followed up on ICU days 0, 5, and 10 with serial cultures of dental plaque (and tracheal aspirates) for aerobic respiratory pathogens, it was found that the percentage of plaque samples with respiratory pathogens increased over time from 23% (13 of 57 samples) to 39% (11 of 28 samples) to 46% (6 of 13 samples), respectively.13 Table 3 of this article reveals acquisition of methicillin-resistant S aureus and pathogenic aerobic Gram-negative rods over time in dental plaques, implying that the plaques are probably picking up these organisms from the surrounding oropharyngeal environment as it becomes populated with these species.13 A focus on the interesting aspect of Table 4 only where the plaque sample culture finding is positive reveals two pneumonias, one with A baumanii and one with P aeruginosa. The positive plaque culture finding predated the tracheal culture and pneumonia. The time sequence suggests dental plaque colonization first with subsequent aspiration of either equilibrating upper airway contents, dislodged dental plaque, or both, and then pneumonia. This is consistent with a substudy13 comparing salivary and dental plaque cultures. They were concordant in 18 of 20 cases implying equilibration of organisms between the dental plaque and the oropharynx in most instances.13

Previous studies14,15 have revealed that in outpatients with severe periodontitis, subgingival Enterobacteriaceae, Pseudomonas, and Acinetobacter are part of the normal flora in 10 to 14% of subjects. In addition, stable nursing home patients have been found to have respiratory pathogens including S aureus, Enterobacter cloacae, and P aeruginosa cultured from dental plaques in 25% of cases.16 These sources may be relatively stable reservoirs harboring respiraton pathogens. Endogenous colonization of the oropharynx and trachea could occur from these sites in patients with poor oral hygiene during an acute illness. Therefore, the possible sources of respiraton pathogens for colonization of the upper airway prior to aspiration and presentation of a hospital-acquired pneumonia include the following: (1) the GI tract in a minority of cases, (2) the teeth themselves, or from (3) the external environment (respiratory therapy equipment, nurses suctioning, etc.).

El-Solh et al, in this issue of CHEST (see page 1575), demonstrate a genetic and bacteriologic match between bronchoscopically obtained BAL respiratory pathogens and dental plaque pathogens. This demonstrates unequivocally that the bacteria- S aureus, Escherichia coli, E cloacae, and P aeruginosa-started in the mouth and went to the lung, since the dental plaque cultures were obtained before the pneumonia developed. One previous study,11 vide supra, found the same genetic match comparing oropharyngeal to BAL samples from VAP as they developed. Neither study answers the following question: Did the oropharynx become colonized first with development of dental plaque colonization, or were respiratory pathogens present on subjects teeth (due to poor dentition and periodontitis), which then colonized the oropharynx when the patients become critically ill? Both studies solidify the concept that proximal airway colonization occurs first with secondary aspiration of these bacteria into the distal airway causing pneumonia.

Edentulous patients, if critically ill, would acquire oropharyngeal colonization with respiratory pathogens even without teeth. This would result in VAP in some patients if they were intubated for other reasons. This then begs the question: Would better oral care of dentate elders prevent or at least reduce the incidence of pneumonia? One study17 attempted to evaluate this question by randomizing 417 elderly nursing home patients without COPD to oral vs no oral care with a 2-year follow-up. The primary outcome variable was the development of pneumonia.17 Ignoring the postrandomization selection bias of 51 dropouts and eliminating the edentulous patients who are not germane to the question (more selection bias), the results were recalculated for the dentate subjects. The relative risk was 1.74 (95% confidence interval, 0.89 to 3.41). This insignificant result suggests there might be a 74% greater chance of developing pneumonia in nursing home patients if they do not receive regular oral care relative to receiving oral care. Consistent with this result, one prospective observational study18 followed up 189 male subject who were at least 60 years old, and noted a 23% increase in the risk of pneumonia over 4 years related to the number of decayed teeth. However, the risk ratio was marginally elevated (odds ratio, 1.23; 955 confidence interval, 1.07 to 1.41), although the study was statistically significant.18 Therefore, the jury is still out on whether or not improving dental hygiene will decrease the risk of pneumonia, although the trend suggests this might be the case.

In conclusion, El Solh et al have added another piece to the pathophysiologic puzzle of how pneumonia develops by demonstrating that VAP can originate from organisms in dental plaque, something that has not been demonstrated before. Like all good studies, it results in asking more questions than it answers. Will improvements in oral hygiene decrease the incidence of pneumonia? Does poor dentition harbor respiratory pathogens that colonize the upper respiratory tract, or does colonization of the respiratory tract result in translocation of bacteria to residual teeth with plaque, or both? Are the edentulous elderly less likely to acquire pneumonia or VAP, and if so should the elderly with a few residual teeth have them removed? The list goes on. Hopefully, with more gains in understand\ing this complex process of colonization and aspiration of respiratory pathogens, we can interrupt the cycle and reduce the incidence of pneumonia and VAP. That time is not yet here.

REFERENCES

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17 Yoneyama T, Yoshida M, Ohrui T, et al. Oral care reduces pneumonia in older patients in nursing homes. J Am Geriatr Soc 2002; 50:430-433

18 Langmore SE, Terpenning MS, Schork A, et al. Predictors of aspiration pneumonia: how important is dysphagia? Dysphagia 1998; 13:69-81

Gene R. Pesola, MD, MPH

New York, NY

Dr. Pesola is Associate Attending, Department of Medicine, Section of Pulmonary/Critical Care Medicine, Harlem Hospital/ Columbia University.

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (e-mail: permissions@chestnet.org).

Correspondence to: Gene R. Pesola, MD, MPH, Department of Medicine, Harlem Hospital/Columbia University, MLK 14101, 506 Lenox Ave, New York, NY 10037; e-mail: grp4@columbia.edu

Copyright American College of Chest Physicians Nov 2004




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