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1.
J Bacteriol ; 201(11)2019 06 01.
Article in English | MEDLINE | ID: mdl-30885933

ABSTRACT

The streptococci are increasingly recognized as a core component of the cystic fibrosis (CF) lung microbiome, yet the role that they play in CF lung disease is unclear. The presence of the Streptococcus milleri group (SMG; also known as the anginosus group streptococci [AGS]) correlates with exacerbation when these microbes are the predominant species in the lung. In contrast, microbiome studies have indicated that an increased relative abundance of streptococci in the lung, including members of the oral microflora, correlates with impacts on lung disease less severe than those caused by other CF-associated microflora, indicating a complex role for this genus in the context of CF. Recent findings suggest that streptococci in the CF lung microenvironment may influence the growth and/or virulence of other CF pathogens, as evidenced by increased virulence factor production by Pseudomonas aeruginosa when grown in coculture with oral streptococci. Conversely, the presence of P. aeruginosa can enhance the growth of streptococci, including members of the SMG, a phenomenon that could be exacerbated by the fact that streptococci are not susceptible to some of the frontline antibiotics used to treat P. aeruginosa infections. Collectively, these studies indicate the necessity for further investigation into the role of streptococci in the CF airway to determine how these microbes, alone or via interactions with other CF-associated pathogens, might influence CF lung disease, for better or for worse. We also propose that the interactions of streptococci with other CF pathogens is an ideal model to study clinically relevant microbial interactions.


Subject(s)
Coinfection/microbiology , Cystic Fibrosis/microbiology , Microbial Interactions/genetics , Pneumococcal Infections/microbiology , Pseudomonas Infections/microbiology , Pseudomonas aeruginosa/genetics , Streptococcus milleri Group/genetics , Anti-Bacterial Agents/therapeutic use , Biofilms/growth & development , Coinfection/pathology , Cystic Fibrosis/drug therapy , Cystic Fibrosis/pathology , Gene Expression , Humans , Lung/microbiology , Lung/pathology , Models, Biological , Pneumococcal Infections/drug therapy , Pneumococcal Infections/pathology , Pseudomonas Infections/drug therapy , Pseudomonas Infections/pathology , Pseudomonas aeruginosa/drug effects , Pseudomonas aeruginosa/growth & development , Pseudomonas aeruginosa/pathogenicity , Streptococcus milleri Group/drug effects , Streptococcus milleri Group/growth & development , Streptococcus milleri Group/pathogenicity , Virulence , Virulence Factors/genetics , Virulence Factors/metabolism
2.
J Bacteriol ; 201(8)2019 04 15.
Article in English | MEDLINE | ID: mdl-30718303

ABSTRACT

Cystic fibrosis (CF) is a genetic disease that causes patients to accumulate thick, dehydrated mucus in the lung and develop chronic, polymicrobial infections due to reduced mucociliary clearance. These chronic polymicrobial infections and subsequent decline in lung function are significant factors in the morbidity and mortality of CF. Pseudomonas aeruginosa and Streptococcus spp. are among the most prevalent organisms in the CF lung; the presence of P. aeruginosa correlates with lung function decline, and the Streptococcus milleri group (SMG), a subgroup of the viridans streptococci, is associated with exacerbations in patients with CF. Here we characterized the interspecies interactions that occur between these two genera. We demonstrated that multiple P. aeruginosa laboratory strains and clinical CF isolates promote the growth of multiple SMG strains and oral streptococci in an in vitro coculture system. We investigated the mechanism by which P. aeruginosa enhances growth of streptococci by screening for mutants of P. aeruginosa PA14 that are unable to enhance Streptococcus growth, and we identified the P. aeruginosapqsL::TnM mutant, which failed to promote growth of Streptococcus constellatus and S. sanguinis Characterization of the P. aeruginosa ΔpqsL mutant revealed that this strain cannot promote Streptococcus growth. Our genetic data and growth studies support a model whereby the P. aeruginosa ΔpqsL mutant overproduces siderophores and thus likely outcompetes Streptococcus sanguinis for limited iron. We propose a model whereby competition for iron represents one important means of interaction between P. aeruginosa and Streptococcus spp.IMPORTANCE Cystic fibrosis (CF) lung infections are increasingly recognized for their polymicrobial nature. These polymicrobial infections may alter the biology of the organisms involved in CF-related infections, leading to changes in growth, virulence, and/or antibiotic tolerance, and could thereby affect patient health and response to treatment. In this study, we demonstrate interactions between P. aeruginosa and streptococci using a coculture model and show that one interaction between these microbes is likely competition for iron. Thus, these data indicate that one CF pathogen may influence the growth of another, and they add to our limited knowledge of polymicrobial interactions in the CF airway.


Subject(s)
Bacterial Proteins/metabolism , Microbial Interactions , Pseudomonas aeruginosa/growth & development , Pseudomonas aeruginosa/metabolism , Siderophores/metabolism , Streptococcus milleri Group/drug effects , Streptococcus milleri Group/growth & development , Bacterial Proteins/genetics , Gene Deletion , Genetic Testing , Iron/metabolism , Mutagenesis, Insertional , Pseudomonas aeruginosa/genetics
3.
Dent Update ; 35(6): 420-4, 2008.
Article in English | MEDLINE | ID: mdl-18717106

ABSTRACT

UNLABELLED: Dental surgeons are faced with treating dental infections on a daily basis and the cases discussed in this paper highlight the potential outcome of such infections, especially in immunocompromised patients. Fulminating infection in the head and neck may present as a rapidly progressive, potentially fatal condition characterized by extensive necrosis of the subcutaneous tissues. One form of such infection is necrotizing fasciitis. Although first described in 1793 by Pouteau, the term necrotizing fasciitis was first coined in 1952 by Wilson who noted that facial necrosis was the most consistent feature of this disease. When necrotizing fasciitis occurs in the head and neck region it is usually odontogenic in origin. This paper reviews the cases of four patients presenting with atypical fulminating dental infection who presented to the oral and maxillofacial department at Guy's and St Thomas's Hospital, London, resulting in cellulitis and necrotizing fasciitis. Aggressive management is critical for patient survival and time wasted is tissue lost. CLINICAL RELEVANCE: Early diagnosis and aggressive treatment of dental infections, especially in patients with altered immune status, is critical. There should be a high index of suspicion in patients with dental infections not responding to treatment and maxillary dental infections with sinus symptoms.


Subject(s)
Cellulitis/etiology , Face , Fasciitis, Necrotizing/etiology , Focal Infection, Dental/complications , Neck/pathology , Adult , Escherichia coli Infections/diagnosis , Humans , Male , Orbital Cellulitis/etiology , Streptococcal Infections/diagnosis , Streptococcus milleri Group/growth & development
4.
Arch Oral Biol ; 53(2): 141-9, 2008 Feb.
Article in English | MEDLINE | ID: mdl-17904095

ABSTRACT

OBJECTIVE: To determine which cell fraction(s) of Streptococcus mitis biovar 1 serve as the best source of antigens recognized by salivary SIgA antibodies in infants. DESIGN: Whole cells of 38 reference and wild-type isolates of S. mitis, Streptococcus oralis, Streptococcus gordonii, Enterococcus casseliflavus, and Enterococcus faecalis were fractionated into cell walls (CW), protease-treated cell walls (PTCW), cell membranes (CM) and cell protein (CP). Whole cells and these fractions were tested for binding by rabbit anti-S. mitis SK145 and anti-S. oralis SK100 sera, and also by salivary SIgA antibodies from infants and adults. RESULTS: Anti-SK145 and anti-SK100 sera bound whole cells and fractions of all strains of S. mitis and S. oralis variably. Cluster analysis of antibody binding data placed the strains into S. mitis, S. oralis and 'non-S. mitis/non-S. oralis' clusters. Antigens from CW and CM best discriminated S. mitis from S. oralis. CM bound the most infant salivary SIgA antibody and PTCW bound the least. In contrast, adult salivary SIgA antibody bound all of the cell fractions and at higher levels. CONCLUSIONS: Presumably the relatively short period of immune stimulation and immunological immaturity in infants, in contrast to adults, result in low levels of salivary SIgA antibody that preferentially bind CM of S. mitis but not PTCW. By utilizing isolated cell walls and membranes as sources of antigens for proteomics it may be possible to identify antigens common to oral streptococci and dissect the fine specificity of salivary SIgA antibodies induced by oral colonization by S. mitis.


Subject(s)
Cell Fractionation/methods , Enterococcus faecalis/immunology , Immunoglobulin A, Secretory/immunology , Saliva/immunology , Streptococcus milleri Group/immunology , Adult , Age Factors , Animals , Antibodies, Bacterial , Binding Sites, Antibody/immunology , Enterococcus faecalis/growth & development , Humans , Immunologic Factors/immunology , Infant , Mouth/microbiology , Rabbits , Saliva/microbiology , Streptococcus milleri Group/growth & development , Streptococcus milleri Group/metabolism
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