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3 results on '"Haemophilus influenzae physiology"'

1. Small-Plasmid-Mediated Antibiotic Resistance Is Enhanced by Increases in Plasmid Copy Number and Bacterial Fitness

Author

Alfonso Santos-Lopez, Rafael Ortega-Huedo, Sean Kennedy, Bruno Gonzalez-Zorn, Cristina Bernabe-Balas, Alvaro San Millan, Facultad de Veterinaria, Universidad Complutense, Universidad Complutense de Madrid = Complutense University of Madrid [Madrid] (UCM), MetaGenoPolis, Institut National de la Recherche Agronomique (INRA), This work was supported by REDEEX-2 (MICINN, BFU 2011-14145-E) and EU projects EvoTAR 282004-FP7 and EFFORT 613754-FP7., We thank E. Frago for help with the statistical analyses and N. Montero for excellent technical assistance., European Project: 282004,EC:FP7:HEALTH,FP7-HEALTH-2011-single-stage,EVOTAR(2011), and European Project: 613754,EC:FP7:KBBE,FP7-KBBE-2013-7-single-stage,EFFORT(2013)

Subjects
MESH: Haemophilus influenzae/drug effects, DNA Copy Number Variations, medicine.drug_class, Antibiotics, MESH: Haemophilus influenzae/physiology, Drug resistance, Biology, MESH: Haemophilus influenzae/genetics, medicine.disease_cause, Microbiology, Haemophilus influenzae, 03 medical and health sciences, Plasmid, Antibiotic resistance, Amp resistance, MESH: Anti-Bacterial Agents/pharmacology, Mechanisms of Resistance, Ampicillin, medicine, Pharmacology (medical), 030304 developmental biology, Pharmacology, Genetics, 0303 health sciences, 030306 microbiology, MESH: Drug Resistance, Microbial/genetics, Drug Resistance, Microbial, biology.organism_classification, Anti-Bacterial Agents, Infectious Diseases, [SDV.MP]Life Sciences [q-bio]/Microbiology and Parasitology, MESH: DNA Copy Number Variations/genetics, Veterinaria, MESH: Plasmids/genetics, Bacteria, medicine.drug, Plasmids
Abstract

Plasmids play a key role in the horizontal spread of antibiotic resistance determinants among bacterial pathogens. When an antibiotic resistance plasmid arrives in a new bacterial host, it produces a fitness cost, causing a competitive disadvantage for the plasmid-bearing bacterium in the absence of antibiotics. On the other hand, in the presence of antibiotics, the plasmid promotes the survival of the clone. The adaptations experienced by plasmid and bacterium in the presence of antibiotics during the first generations of coexistence will be crucial for the progress of the infection and the maintenance of plasmid-mediated resistance once the treatment is over. Here we developed a model system using the human pathogen Haemophilus influenzae carrying the small plasmid pB1000 conferring resistance to β-lactam antibiotics to investigate host and plasmid adaptations in the course of a simulated ampicillin therapy. Our results proved that plasmid-bearing clones compensated for the fitness disadvantage during the first 100 generations of plasmid-host adaptation. In addition, ampicillin treatment was associated with an increase in pB1000 copy number. The augmentation in both bacterial fitness and plasmid copy number gave rise to H. influenzae populations with higher ampicillin resistance levels. In conclusion, we show here that the modulations in bacterial fitness and plasmid copy number help a plasmid-bearing bacterium to adapt during antibiotic therapy, promoting both the survival of the host and the spread of the plasmid.

Published
2015

2. Pathogen Diversity and Hidden Regimes of Apparent Competition

Author

Cobey, Sarah and Lipsitch, Marc

Subjects
genetic fitness, haemophilus infections/immunology, haemophilus infections/microbiology*, haemophilus influenzae/physiology*, humans, microbial interactions, models, biological, pneumococcal infections/immunology*, pneumococcal infections/microbiology*, population dynamics, species specificity, streptococcus pneumoniae/genetics, streptococcus pneumoniae/physiology*, apparent competition, pneumococcus, Haemophilus influenzae, microbiome, immunity, pathogen
Abstract

Competition through cross-reacting host immune responses, a form of apparent competition, is a major driver of pathogen evolution and diversity. Most models of pathogens have focused on intraspecific interactions to explain observed patterns. Two recent experiments suggested that Haemophilus influenzae, a common nasopharyngeal colonizer of humans, might alter the immune environment in a way that favors otherwise less fit serotypes of another common pathogen, pneumococcus. Using a computational model, we demonstrate that H. influenzae, if it consistently raises the fitness of the less fit serotypes, can strongly promote pneumococcal diversity. However, the effects of H. influenzae are so sensitive to the prevalence of H. influenzae that this species is unlikely to be the main driver of serotype coexistence. Interactions that significantly affect diversity could furthermore be extremely difficult to detect through co-occurrence analysis alone. These results suggest that small differences in strains' adaptations to different immunological regimes, which are shaped by coinfections with other pathogens, can have dramatic effects on strain dynamics and patterns of phenotypic variation. Studies of microbial communities might therefore benefit from the use of varied approaches to infer the presence of indirect interactions.

Published
2013
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3. Microbial interactions in the respiratory tract.

Author

Murphy, Timothy F, Bakaletz, Lauren O, Smeesters, Pierre, Murphy, Timothy F, Bakaletz, Lauren O, and Smeesters, Pierre

Abstract

Upper respiratory tract infections are caused by the synergistic and antagonistic interactions between upper respiratory tract viruses and 3 predominant bacterial pathogens: Streptococcus pneumoniae, nontypeable Haemophilus influenzae (NTHi), and Moraxella catarrhalis, which are members of the commensal flora of the nasopharynx. For many bacterial pathogens, colonization of host mucosal surfaces is a first and necessary step in the infectious process. S. pneumoniae and H. influenzae have intricate interactions in the nasopharynx. The host innate immune response may influence these interactions and therefore influence the composition of the colonizing flora and the invading bacteria. S. pneumoniae, nontypeable H. influenzae, and M. catarrhalis can behave as opportunistic pathogens of the middle ear when conditions are optimal. Chronic otitis media (OM) and recurrent OM include a biofilm component. Each of the 3 predominant pathogens of OM can form a biofilm and have been shown to comprise biofilms present on middle ear mucosa specimens recovered from children with recurrent or chronic OM. Some of these characterized biofilms are of mixed bacterial etiology, suggesting that progress made on single-microbe directed strategies for treatment and/or prevention of OM, although highly encouraging, are likely to be inadequate. A significantly greater understanding about microbial physiology is required as it relates to the involvement of biofilms in OM, to identify points in the natural course of the disease that are perhaps more amenable to treatment strategies, as well as to identify biofilm-relevant antigenic targets that would be helpful in the rational design of vaccines to prevent OM., Journal Article, Review, SCOPUS: re.j, info:eu-repo/semantics/published

Published
2009

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