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Biomedical subjects

F A Scannapieco

Publications and source records attributed to F A Scannapieco.

At least 19 recordsLinked to original sources
PubMed2003

Amylase-binding proteins A (AbpA) and B (AbpB) differentially affect colonization of rats' teeth by Streptococcus gordonii.

Streptococcus gordonii produces two alpha-amylase-binding proteins, AbpA and AbpB, that have been extensively studied in vitro. Little is known, however, about their significance in oral colonization and cariogenicity (virulence). To clarify these issues, weanling specific pathogen-free Osborne-Mendel rats, TAN : SPFOM(OM)BR, were inoculated either with wild-type strains FAS4-S or Challis-S or with strains having isogenic mutations of abpA, abpB, or both, to compare their colonization abilities and persistence on the teeth. Experiments were done with rats fed a sucrose-rich diet containing low amounts of starch or containing only starch. The mutants and wild-types were quantified in vivo and carious lesions were scored. In 11 experiments, S. gordonii was a prolific colonizer of the teeth when rats were fed the sucrose (with low starch)-supplemented diet, often dominating the flora. Sucrose-fed rats had several-fold higher recoveries of inoculants than those eating the sucrose-free, starch-supplemented diet, regardless of inoculant type. The strain defective in AbpB could not colonize teeth of starch-only-eating rats, but could colonize rats if sucrose was added to the diet. Strains defective in AbpA surprisingly colonized better than their wild-types. A double mutant deficient in both AbpA and AbpB (abpA/abpB) colonized like its wild-type. Wild-types FAS4-S and Challis-S had no more than marginal cariogenicity. Notably, in the absence of AbpA, cariogenicity was slightly augmented. Both the rescue of colonization by the AbpB- mutant and the augmentation of colonization by AbpA- mutant in the presence of dietary sucrose suggested additional amylase-binding protein interactions relevant to colonization. Glucosyltransferase activity was greater in mutants defective in abpA and modestly increased in the abpB mutant. It was concluded that AbpB is required for colonization of teeth of starch-eating rats and its deletion is partially masked if rats eat a sucrose-starch diet. AbpA appears to inhibit colonization of the plaque biofilm in vivo. This unexpected effect in vivo may be associated with interaction of AbpA with glucosyltransferase or with other colonization factors of these cells. These data illustrate that the complex nature of the oral environment may not be adequately modelled by in vitro systems.

Animals↗
PubMed2001

Oral colonization and cariogenicity of Streptococcus gordonii in specific pathogen-free TAN:SPFOM(OM)BR rats consuming starch or sucrose diets.

The significance of Streptococcus gordonii in dental caries is undefined, as is that of other alpha-amylase-binding bacteria (ABB) commonly found in the mouth. To clarify the ecological and cariological roles of S. gordonii our specific pathogen-free Osborne-Mendel rats, TAN:SPFOM(OM)BR, were fed either diet 2000 (containing 56% confectioner's sugar, most of which is sucrose) or diet 2000CS (containing 56% cornstarch, in lieu of confectioner's sugar) and inoculated with S. gordonii strains. Uninoculated rats were free of both indigenous mutans streptococci (MS) and ABB, including S. gordonii, as shown by culture on mitis salivarius and blood agars of swabs and sonicates of dentitions after weanlings had consumed these diets for 26 days. ABB were detected by radiochemical assay using [125I]-amylase reactive to alpha-amylase-binding protein characteristic of the surface of S. gordonii and other ABB. No ABB were detected (detection limit < 1 colony-forming units in 10(6) colony-forming units). Thus the TAN:SPFOM(OM)BR colony presents a 'clean animal model' for subsequent study. Consequently, S. gordonii strains Challis or G9B were used to inoculate weanling rat groups consuming either the high-sucrose diet 2000 or the cornstarch diet 2000CS. Two additional groups fed each of these diets remained unioculated. Recoveries of inoculants were tested 12 and 26 days later by oral swabs and sonication of the molars of one hemimandible of each animal, respectively. Uninoculated animals were reconfirmed to be free of ABB and mutans streptococci, but inoculated ones eating diet 2000CS had S. gordonii recoveries of 1-10% or, if eating diet 2000, 10-30% of total colony-farming units in sonicates. There were no statistically significant differences among the inoculated and uninoculated animal groups' caries scores when they ate the cornstarch diet. Lesion scores for sucrose-eating rats were, however, from 2.4-5.1-fold higher than for cornstarch-eating rats, P < 0.001, and were still higher if animals had been inoculated with either Challis (1.41-fold) or G9B (1.64-fold), than if uninoculated, both P < 0.001, so long as the rats ate the sucrose diet. Therefore, TAN:SPFOM(OM)BR rats do not harbour ABB or S. gordonii but can be colonized by S. gordonii. Colonization levels of S. gordonii on the teeth are higher in the presence of high sucrose than with high starch-containing diets. Caries scores are augmented by sucrose compared with starch, and are further augmented by S gordonii colonization. S. gordonii is thus cariologically significant in the presence of sucrose, at least in this rat.

Amylases↗
PubMed2001

Role of Streptococcus gordonii amylase-binding protein A in adhesion to hydroxyapatite, starch metabolism, and biofilm formation.

Interactions between bacteria and salivary components are thought to be important in the establishment and ecology of the oral microflora. alpha-Amylase, the predominant salivary enzyme in humans, binds to Streptococcus gordonii, a primary colonizer of the tooth. Previous studies have implicated this interaction in adhesion of the bacteria to salivary pellicles, catabolism of dietary starches, and biofilm formation. Amylase binding is mediated at least in part by the amylase-binding protein A (AbpA). To study the function of this protein, an erythromycin resistance determinant [erm(AM)] was inserted within the abpA gene of S. gordonii strains Challis and FAS4 by allelic exchange, resulting in abpA mutant strains Challis-E1 and FAS4-E1. Comparison of the wild-type and mutant strains did not reveal any significant differences in colony morphology, biochemical metabolic profiles, growth in complex or defined media, surface hydrophobicity, or coaggregation properties. Scatchard analysis of adhesion isotherms demonstrated that the wild-type strains adhered better to human parotid-saliva- and amylase-coated hydroxyapatite than did the AbpA mutants. In contrast, the mutant strains bound to whole-saliva-coated hydroxyapatite to a greater extent than did the wild-type strains. While the wild-type strains preincubated with purified salivary amylase grew well in defined medium with potato starch as the sole carbohydrate source, the AbpA mutants did not grow under the same conditions even after preincubation with amylase. In addition, the wild-type strain produced large microcolonies in a flow cell biofilm model, while the abpA mutant strains grew much more poorly and produced relatively small microcolonies. Taken together, these results suggest that AbpA of S. gordonii functions as an adhesin to amylase-coated hydroxyapatite, in salivary-amylase-mediated catabolism of dietary starches and in human saliva-supported biofilm formation by S. gordonii.

Adhesins, Bacterial↗
PubMed2001

RegG, a CcpA homolog, participates in regulation of amylase-binding protein A gene (abpA) expression in Streptococcus gordonii.

The amylase-binding protein A (AbpA) of Streptococcus gordonii was found to be undetectable in supernatants of mid-log-phase cultures containing >1% glucose but abundant in supernatants of cultures made with brain heart infusion (BHI), which contains 0.2% glucose. A 10-fold decrease in the level of abpA mRNA in S. gordonii cells cultured in BHI was noted after the addition of glucose to 1%. Analysis of the abpA sequence revealed a potential catabolite responsive element CRE 153 bp downstream of the putative translational start site. A catabolite control protein A gene (ccpA) homolog from S. gordonii, designated regG, was cloned. A regG mutant strain demonstrated moderately less repression of abpA transcription in the presence of 1% glucose. Diauxic growth with glucose and lactose was not affected in the RegG mutant compared to the wild-type parental strain. These results suggest that while RegG plays a role in abpA expression, other mechanisms of catabolite repression are present.

Amino Acid Sequence↗
PubMed2001

Oral bacteria and respiratory infection: effects on respiratory pathogen adhesion and epithelial cell proinflammatory cytokine production.

Several microbiologic and epidemiologic studies have suggested an association between dental plaque, poor oral health, and respiratory diseases such as nosocomial pneumonia and chronic obstructive pulmonary disease (COPD). A number of hypotheses are suggested to help explain how oral bacteria may participate in the pathogenesis of respiratory infection. Resident bacteria in oral secretions are likely aspirated along with respiratory pathogens and may affect the adhesion of the later organisms to the respiratory epithelium. Preliminary studies performed in our laboratory suggest that oral bacteria may modulate the adhesion of respiratory pathogens to epithelial cell lines. In addition, oral bacterial products or cytokines in oral/pharyngeal aspirates may stimulate cytokine production from respiratory epithelial cells, resulting in recruitment of inflammatory cells. The resulting inflamed epithelium may be more susceptible to respiratory infection. Further preliminary data are presented that some species of oral bacteria may induce the release of proinflammatory cytokines from epithelial cell lines to an extent similar to that seen for respiratory pathogens.

Aggregatibacter actinomycetemcomitans↗
PubMed2001

Potential associations between chronic respiratory disease and periodontal disease: analysis of National Health and Nutrition Examination Survey III.

BACKGROUND: Associations between poor oral health and chronic lung disease have recently been reported. The present study evaluated these potential associations by analyzing data from the National Health and Nutrition Examination Survey III (NHANES III), which documents the general health and nutritional status of randomly selected United States subjects from 1988 to 1994. METHODS: This cross-sectional, retrospective study of the NHANES III database included a study population of 13,792 subjects > or = 20 years of age with at least 6 natural teeth. A history of bronchitis and/or emphysema was recorded from the medical questionnaire, and a dichotomized variable combined those with either chronic bronchitis and/or emphysema, together considered as chronic obstructive pulmonary disease (COPD). Subject lung function was estimated by calculating the ratio of forced expiratory volume (FEV) after 1 second (FEV1)/forced vital capacity (FVC). Oral health status was assessed from the DMFS/T index (summary of cumulative caries experience), gingival bleeding, gingival recession, gingival probing depth, and periodontal attachment level. Unweighted analyses were used for initial examination of the data, and a weighted analysis was performed in a final logistic regression model adjusting for age, gender, race and ethnicity, education, income, frequency of dental visits, diabetes mellitus, smoking, and alcohol use. RESULTS: The mean age of all subjects was 44.4 +/- 17.8 years (mean +/- SD): COPD = 51.2 +/- 17.9 years and subjects without COPD = 43.9 +/- 17.7 years. Subjects with a history of COPD had more periodontal attachment loss than subjects without COPD (1.48 +/- 1.35 mm versus 1.17 +/- 1.09 mm, P = 0.0001). Subjects with mean attachment loss (MAL) > or = 3.0 mm had a higher risk of COPD than those having MAL < 3.0 mm (odds ratio, 1.45; 95% CI, 1.02 to 2.05). A trend was noted in that lung function appeared to diminish with increasing periodontal attachment loss. CONCLUSIONS: The findings of the present analysis support recently published reports that suggest an association between periodontal disease and COPD.

Adult↗
PubMed1999

The risk of nosocomial pneumonia is not increased during partial liquid ventilation.

OBJECTIVE: To determine whether partial liquid ventilation (PLV) affects the risk of nosocomial pneumonia. STUDY DESIGN: To assess in vitro bacterial adhesion and viability after liquid perfluorocarbon exposure and to assess bacterial recovery after partial liquid ventilation in vivo in rabbits. SETTING: University animal research facility. SUBJECTS: Thirty-six New Zealand White rabbits. INTERVENTIONS: To assess adhesions, radiolabeled Escherichia coli were exposed to perfluorocarbon, incubated against artificial biosurfaces, and compared with nonexposed controls. Bacterial viability in vitro was assessed by exposing broth suspensions of Pasteurella multocida to perflubron for various times. Controls were run in parallel without exposure. Quantitative cultures were performed to determine viability. We undertook short-term and recovery in vivo investigations. The lungs of treated animals were filled with perflubron (approximately 18 mL/kg), and the control rabbits were ventilated without perflubron in an identical fashion. Cryopreserved aliquots of P. multocida were administered via an endotracheal tube. The short-term study animals were ventilated for 6 hrs before being killed. The recovery animals were ventilated for 2-4 hrs, extubated, and killed 20 hrs later. The lungs were removed, aseptically minced, and homogenized. Serial dilutions of the homogenate were quantitatively cultured by manual counting of colonies on agar plates. The recovered organisms were typed for species by the clinical microbiology laboratory. MEASUREMENTS AND MAIN RESULTS: The adhesion of bacteria to immobilized bronchoalveolar lavage and human saliva, respectively, was reduced by 65%+/-7% and 66%+/-1% (p < .05; n = 5) after exposure to perflubron and by 63%+/-9% and 68%+/-6% after exposure to FC-77 (p < .05; n = 5); however, adhesion was not affected by exposure to Rimar. There was no difference in bacterial viability between the control and perflubron-exposed bacteria (n = 5). The in vivo study demonstrated a ten-fold or greater reduction in the number of recovered bacteria in the partial liquid ventilated group compared with the control group. CONCLUSIONS: This study suggests that different perfluorocarbons affect adhesions differently. Perflubron and FC-77 appear to decrease bacterial adhesion, whereas Rimar does not. Rerflubron does not have a direct bactericidal effect. Furthermore, PLV with perflubron decreased the number of viable bacteria per gram of tissue after an intentional inoculation of the airway, suggesting that the risk of nosocomial pneumonia is unlikely to be increased during PLV and may, in fact, be reduced in patients supported with PLV.

Animals↗
PubMed1999

Association of periodontal infections with atherosclerotic and pulmonary diseases.

Chronic infections may influence the severity and/or course of a number of systemic diseases. Periodontal diseases are localized chronic inflammatory conditions of the gingiva and underlying bone and connective tissues induced by bacteria and bacterial products of dental plaque. This paper will discuss the evidence for the role of periodontal disease in the pathogenesis of 2 important systemic diseases, atherosclerosis and pulmonary infections. Both epidemiological and laboratory studies are reviewed to assess the biological basis for the association of periodontal infections and these important diseases. Several potential mechanisms by which periodontal diseases may influence these conditions are also discussed.

Alveolar Process↗
PubMed1999

Identification and molecular analysis of rough-colony-specific outer membrane proteins of Actinobacillus actinomycetemcomitans.

Actinobacillus actinomycetemcomitans, a gram-negative bacterium isolated from the human mouth, has been implicated in the pathogenesis of early-onset periodontitis. Primary isolates cultured from subgingival plaque exhibit an adherent, rough colony phenotype which spontaneously converts to a nonadherent, smooth phenotype upon in vitro subculture. The rough colony variant produces abundant fimbriae and autoaggregates, while the smooth colony variant is planktonic and produces scant fimbriae. To begin to understand the significance of colony variation in biofilm formation by A. actinomycetemcomitans, outer membrane protein profiles of four isogenic rough and smooth colony variants were compared by sodium dodecyl sulfate-polyacrylamide gel electrophoresis. Two proteins with relative molecular masses of 43 and 20 kDa were expressed by the rough colony variants exclusively. Expression of these proteins was not found to be dependent on growth phase, oxygen tension, or type of complex medium. N-terminal amino acid sequences of these proteins obtained by Edman degradation were compared with sequences from the University of Oklahoma A. actinomycetemcomitans genome database. Two contiguous open reading frames (ORFs) encoding proteins having sequence homology with these proteins were identified. The 43-kDa protein (RcpA [rough colony protein A]) was similar to precursor protein D of the general secretion pathway of gram-negative bacilli, while the 20-kDa protein (RcpB [rough colony protein B]) appeared to be unique. The genes encoding these proteins have been cloned from A. actinomycetemcomitans 283 and sequenced. A BLASTX (gapped BLAST) search of the surrounding ORFs revealed homology with other fimbria-related proteins. These data suggest that the genes encoding the 43-kDa (rcpA) and 20-kDa (rcpB) proteins may be functionally related to each other and to genes that may encode fimbria-associated proteins.

Aggregatibacter actinomycetemcomitans↗
PubMed1999

Prevalence of the amylase-binding protein A gene (abpA) in oral streptococci.

Salivary amylase binds specifically to a number of oral streptococcal species. This interaction may play an important role in dental plaque formation. Recently, a 585-bp gene was cloned and sequenced from Streptococcus gordonii Challis encoding a 20.5-kDa amylase-binding protein (AbpA). The goal of this study was to determine if related genes are present in other species of oral streptococci. Biotinylated abpA was used in Southern blot analysis to screen genomic DNA from several strains representing eight species of oral streptococci. This probe hybridized with a 4.0-kb HindIII restriction fragment from all 13 strains of S. gordonii tested. The probe did not appear to bind to any restriction fragments from other species of amylase-binding oral streptococci including Streptococcus mitis (with the exception of 1 of 14 strains), Streptococcus crista (3 strains), Streptococcus anginosus (1 strain), and Streptococcus parasanguinis (1 strain), or to non-amylase-binding oral streptococci including Streptococcus sanguinis (3 strains), Streptococcus oralis (4 strains), and Streptococcus mutans (1 strain). Primers homologous to sequences within the 3' and 5' ends of abpA yielded products of 400 bp following PCR of genomic DNA from the Southern blot-positive strains. Several of these PCR products were cloned and sequenced. The levels of similarity of these cloned products to the abpA of S. gordonii Challis ranged from 91 to 96%. These studies reveal that the abpA gene appears to be specific to S. gordonii and differs from genes encoding amylase-binding proteins from other species of amylase-binding streptococci.

Amylases↗
PubMed1999

Role of oral bacteria in respiratory infection.

An association between oral conditions such as periodontal disease and several respiratory conditions has been noted. For example, recent evidence has suggested a central role for the oral cavity in the process of respiratory infection. Oral periodontopathic bacteria can be aspirated into the lung to cause aspiration pneumonia. The teeth may also serve as a reservoir for respiratory pathogen colonization and subsequent nosocomial pneumonia. Typical respiratory pathogens have been shown to colonize the dental plaque of hospitalized intensive care and nursing home patients. Once established in the mouth, these pathogens may be aspirated into the lung to cause infection. Other epidemiologic studies have noted a relationship between poor oral hygiene or periodontal bone loss and chronic obstructive pulmonary disease. Several mechanisms are proposed to explain the potential role of oral bacteria in the pathogenesis of respiratory infection: 1. aspiration of oral pathogens (such as Porphyromonas gingivalis, Actinobacillus actinomycetemcomitans, etc.) into the lung to cause infection; 2. periodontal disease-associated enzymes in saliva may modify mucosal surfaces to promote adhesion and colonization by respiratory pathogens, which are then aspirated into the lung; 3. periodontal disease-associated enzymes may destroy salivary pellicles on pathogenic bacteria to hinder their clearance from the mucosal surface; and 4. cytokines originating from periodontal tissues may alter respiratory epithelium to promote infection by respiratory pathogens.

Aggregatibacter actinomycetemcomitans↗
PubMed1998

Associations between oral conditions and respiratory disease in a national sample survey population.

Respiratory infectious diseases such as bacterial pneumonia and bronchitis are common and costly, especially in institutionalized and elderly inpatients. Respiratory infection is thought to rely in part on the aspiration of oropharyngeal flora into the lower respiratory tract and failure of host defense mechanisms to eliminate the contaminating bacteria, which then multiply to cause infection. It has been suggested that dental plaque may act as a reservoir of respiratory pathogens, especially in patients with periodontal disease. However, the impact of poor oral health on oral respiratory pathogen colonization and lung infection is uncertain, especially in ambulatory, non-institutionalized populations. To begin to assess potential associations between respiratory diseases and oral health, data from the National Health and Nutrition Examination Survey I (NHANES I) were analyzed. This database contains information on the general health status of 23,808 individual Of these, 386 individuals reported a suspected respiratory condition that was further assessed by a physician. These subjects were categorized as having a confirmed chronic respiratory disease (chronic bronchitis or emphysema) or an acute respiratory disease (influenza, pneumonia, acute bronchitis). They were compared to those not having a respiratory disease. Initial non-parametric analysis noted that individuals with a confirmed chronic respiratory disease (n = 41) had significantly greater oral hygiene index scores than subjects without respiratory disease (n = 193; P = 0.0441). Logistic regression analysis of data from these subjects, which considered age, race, gender, smoking status, and simplified oral hygiene index (OHI), suggested that subjects having the median OHI value were 1.3 times more likely to have a chronic respiratory disease relative to those with and OHI of O. Similarly, subjects with the maximum OHI value were 4.5 times more likely to have a chronic respiratory disease than those with an OHI of O. No evidence was found to support an association between the periodontal index and any respiratory disease. These results suggest OHI to have a residual effect on chronic respiratory disease of both practical and statistical significance.

Acute Disease↗
PubMed1998

Position paper of The American Academy of Periodontology: periodontal disease as a potential risk factor for systemic diseases.

This paper on periodontal disease as a potential risk factor for systemic diseases was prepared by the Research, Science and Therapy Committee of The American Academy of Periodontology. It is intended to provide information regarding the role of periodontal disease in systemic diseases, including bacteremia, infective endocarditis, cardiovascular disease and atherosclerosis, prosthetic device infection, diabetes mellitus, respiratory diseases, and adverse pregnancy outcomes.

Arteriosclerosis↗
PubMed1997

The microbial ecology and immunology of the adenoid: implications for otitis media.

The nasopharyngeal tonsil, or adenoid, is a major inductive site for the synthesis of J-chain-positive B cells that may migrate to other areas of the upper respiratory tract, such as the nasal mucosa, the parotid gland, the lacrimal gland, and the middle ear during inflammation. The production of secretory IgA by both the nasopharyngeal tonsil and the nasal mucosa plays a major role in local immune protection against bacteria and viruses. The release of cytokines from Th1 and Th2 lymphocytes must be appropriate for B cells to produce IgA. The factors or mechanisms responsible for this are not, at present, known, but it appears that there is a difference in the profiles of cytokine secretion by Th1 and Th2 lymphocytes in the adenoids in both otitis-prone, as well as nonotitis-prone children. We have suggested that if this specific immune system does not protect the host from invasion by potential pathogens, there are other modalities of therapy to protect the nasopharynx from colonization with pathogenic bacteria or viruses. These include the production of specific antibodies against bacterial surface proteins that have been identified as mucin-binding proteins. Alteration of the microbial flora with commensal organisms such as viridans streptococci can be utilized. These alpha-hemolytic streptococci probably function by producing an acid environment that prevents colonization of organisms such as nontypeable H. influenzae. Finally, the induction of specific SIgA by conserved outer membrane protein antigens of potential pathogens may be another strategy in the prevention of colonization of potential bacterial pathogens in the nasopharynx.

Adenoids↗
PubMed1996

Role of type 1 fimbriae in the adhesion of Escherichia coli to salivary mucin and secretory immunoglobulin A.

Saliva is known to modulate the adhesion of bacteria in the oral cavity. The present work was performed to assess the effect of salivary components on the adhesion of Escherichia coli to a model oral surface. Several genetically engineered E. coli strains were used to examine the role of type 1 fimbriation in the interaction of these strains with salivary components in solution or adsorbed to hydroxyapatite. High (MG1) and low (MG2) molecular weight salivary mucins, and secretory immunoglobulin A (sIgA), were found to interact with the surface of E. coli, and these interactions were independent of the expression of fimbriae or capsule. In contrast, fimbriated strains of E. coli adhered to a greater extent to saliva-coated synthetic hydroxyapatite (HAP) than did nonfimbriated strains. Testing of salivary components separated by gel filtration chromatography revealed that only high-molecular-weight components promoted adhesion of E. coli to HAP. Additional studies found that purified MG2 and sIgA promoted the adhesion of E. coli to HAP. Expression of type 1 fimbriae enhanced adhesion, while mannose inhibited adhesion of fimbriated strains, to saliva-coated HAP and to HAP coated with MG2 and sIgA. We conclude that salivary MG2 and sIgA may provide receptors for the adhesion of type 1 fimbriated E. coli to oral surfaces.

Bacterial Adhesion↗
PubMed1996

Relationships between periodontal disease and bacterial pneumonia.

Bacterial pneumonia is a prevalent and costly infection that is a significant cause of morbidity and mortality in patients of all ages. The continuing emergence of antibiotic-resistant bacteria (e.g., penicillin-resistant pneumococci) suggests that bacterial pneumonia will assume increasing importance in the coming years. Thus, knowledge of the pathogenesis of, and risk factors for, bacterial pneumonia is critical to the development of strategies for prevention and treatment of these infections. Bacterial pneumonia in adults is the result of aspiration of oropharyngeal flora into the lower respiratory tract and failure of host defense mechanisms to eliminate the contaminating bacteria, which multiply in the lung and cause infection. It is recognized that community-acquired pneumonia and lung abscesses can be the result of infection by anaerobic bacteria; dental plaque would seem to be a logical source of these bacteria, especially in patients with periodontal disease. It is also possible that patients with high risk for pneumonia, such as hospitalized patients and nursing home residents, are likely to pay less attention to personal hygiene than healthy patients. One important dimension of this personal neglect may be diminished attention to oral hygiene. Poor oral hygiene and periodontal disease may promote oropharyngeal colonization by potential respiratory pathogens (PRPs) including Enterobacteriaceae (Klebsiella pneumoniae, Escherichia coli, Enterobacter species, etc.), Pseudomonas aeruginosa, and Staphylococcus aureus. This paper provides the rationale for the development of this hypothesis especially as it pertains to mechanically ventilated intensive care unit patients and nursing home residents, two patient groups with a high risk for bacterial pneumonia.

Adult↗