Pseudomonas aeruginosa  Type III Secretion System Virulotypes and Their Association with Clinical Features of Cystic Fibrosis Patients

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Abstract

Purpose

Pseudomonas aeruginosa appears as the main pathogen in cystic fibrosis (CF) involved in recurrent pneumonia and pulmonary exacerbations. The type III secretion system (T3SS) is one of its main determinants of virulence and is associated with poor clinical progression and increased mortality. This study determined the relationship of clinical features of patients with CF and P. aeruginosa T3SS virulotypes.

Materials and Methods

From January 2018 to March 2019, P. aeruginosa were isolated from sputum and/or oropharyngeal swabs. T3SS markers ( exoS, exoU, exoT and exoY) were detected by PCR. Clinical severity according to Shwachman-Kulckycki score and spirometry data were associated with T3SS virulotypes.

Results

A total of 49 patients had positive cultures for P. aeruginosa. T3SS virulence-related markers were detected as follows: exoS 97.9% (n=48), exoU 63.2% (n=31), exoT 95.9% (n=47) and exoY 97.9% (n=48). The prevalence of exoS ⁺/exoU ⁺ virulotype was higher than previously reported in CF settings, being detected in 61.2% of the evaluated isolates, present in 70% of intermittent infections and with a significantly higher frequency in cases of exacerbations. The presence of exoU in chronic infection was not associated with poor clinical results. In chronic infections, the exoS ⁺/exoU ⁻ virulotype prevailed (77.8%) and was associated to worse clinical results according to the Shwachman-Kulckycki score and spirometric.

Conclusion

Our findings revealed a high prevalence of the atypical exoS ⁺/exoU ⁺ virulotype among P. aeruginosa isolates from patients with CF, which was associated with intermittent infection and early clinical alterations, while the exoS ⁺/exoU ⁻ virulotype was associated with chronic infection and worse clinical results. Finally, the presented data highlight the relevance of T3SS virulence markers in the clinical progression and disease severity in CF patients.

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Most cited references 36

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Cystic fibrosis.

J. Elborn (2016)

Cystic fibrosis is a common life-limiting autosomal recessive genetic disorder, with highest prevalence in Europe, North America, and Australia. The disease is caused by mutation of a gene that encodes a chloride-conducting transmembrane channel called the cystic fibrosis transmembrane conductance regulator (CFTR), which regulates anion transport and mucociliary clearance in the airways. Functional failure of CFTR results in mucus retention and chronic infection and subsequently in local airway inflammation that is harmful to the lungs. CFTR dysfunction mainly affects epithelial cells, although there is evidence of a role in immune cells. Cystic fibrosis affects several body systems, and morbidity and mortality is mostly caused by bronchiectasis, small airways obstruction, and progressive respiratory impairment. Important comorbidities caused by epithelial cell dysfunction occur in the pancreas (malabsorption), liver (biliary cirrhosis), sweat glands (heat shock), and vas deferens (infertility). The development and delivery of drugs that improve the clearance of mucus from the lungs and treat the consequent infection, in combination with correction of pancreatic insufficiency and undernutrition by multidisciplinary teams, have resulted in remarkable improvements in quality of life and clinical outcomes in patients with cystic fibrosis, with median life expectancy now older than 40 years. Innovative and transformational therapies that target the basic defect in cystic fibrosis have recently been developed and are effective in improving lung function and reducing pulmonary exacerbations. Further small molecule and gene-based therapies are being developed to restore CFTR function; these therapies promise to be disease modifying and to improve the lives of people with cystic fibrosis.

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Pseudomonas aeruginosa: new insights into pathogenesis and host defenses.

Robert E. W. Hancock, Shaan Gellatly (2013)

Pseudomonas aeruginosa is a metabolically versatile bacterium that can cause a wide range of severe opportunistic infections in patients with serious underlying medical conditions. These infections are characterized by an intense neutrophilic response resulting in significant damage to host tissues and often exhibit resistance to antibiotics leading to mortality. Treatment of persistent infections is additionally hampered by adaptive resistance, due to the growth state of the bacterium in the patient including the microorganism's ability to grow as a biofilm. An array of P. aeruginosa virulence factors counteract host defences and can cause direct damage to host tissues or increase the bacterium's competitiveness. New prevention and treatment methods are urgently required to improve the outcome of patients with P. aeruginosa infections. This review describes the two main types of P. aeruginosa lung infections and provides an overview of the host response and how the genomic capacity of P. aeruginosa contributes to the pathogenesis and persistence of these infections. © 2013 Federation of European Microbiological Societies. Published by Blackwell Publishing Ltd. All rights reserved.

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Prevalence of type III secretion genes in clinical and environmental isolates of Pseudomonas aeruginosa.

H Feltman, G Schulert, Marnie L. Peterson … (2001)

The type III secretion system of Pseudomonas aeruginosa transports four known effector proteins: ExoS, ExoT, ExoU and ExoY. However, the prevalence of the type III secretion system genes or the effector-encoding genes in clinical and environmental isolates of P. aeruginosa has not been well studied. Southern hybridization analyses and PCR were performed on over 100 P. aeruginosa isolates to determine the distribution of these genes. Clinical isolates were obtained from urine, endotracheal, blood and wound specimens, from the sputum of cystic fibrosis (CF) patients, and from non-hospital environmental sites. The popB gene was used as a marker for the presence of the large chromosomal locus encoding the type III secretion machinery proteins. Each isolate contained the popB gene, indicating that at least a portion of this large chromosomal locus was present in all isolates. Likewise, each isolate contained exoT-like sequences. In contrast, the exoS, exoU and exoY genes were variable traits. Overall, 72% of examined isolates contained the exoS gene, 28% contained the exoU gene, and 89% contained the exoY gene. Interestingly, an inverse correlation was noted between the presence of the exoS and exoU genes in that all isolates except two contained either exoS or exoU but not both. No significant difference in exoS, exoU or exoY prevalence was observed between clinical and environmental isolates or between isolates cultured from different disease sites except for CF respiratory isolates. CF isolates harboured the exoU gene less frequently and the exoS gene more frequently than did isolates from some of the other sites of infection, including the respiratory tract of patients without CF. These results suggest that the P. aeruginosa type III secretion system is present in nearly all clinical and environmental isolates but that individual isolates and populations of isolates from distinct disease sites differ in their effector genotypes. The ubiquity of type III secretion genes in clinical isolates is consistent with an important role for this system in human disease.

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Author and article information

Journal

Journal ID (nlm-ta): Infect Drug Resist

Journal ID (iso-abbrev): Infect Drug Resist

Journal ID (publisher-id): idr

Journal ID (pmc): idr

Title: Infection and Drug Resistance

Publisher: Dove

ISSN (Electronic): 1178-6973

Publication date (Electronic): 22 October 2020

Publication date Collection: 2020

Volume: 13

Pages: 3771-3781

Affiliations

[1 ]Programa de Pós-graduação em Biologia Parasitária na Amazônia, Universidade do Estado do Pará , Belém, Pará, Brazil

[2 ]Hospital Universitário João de Barros Barreto, Universidade Federal do Pará , Belém, Pará, Brazil

[3 ]Mestrado Profissional em Ensino em Saúde – Educação Médica, Centro Universitário do Pará , Belém, Pará, Brazil

[4 ]Instituto Evandro Chagas, Seção de Bacteriologia e Micologia , Ananindeua, Pará, Brazil

Author notes

Correspondence: Edilene do Socorro Nascimento Falcão Sarges Ambulatório de Fibrose Cística, Hospital Universitário João de Barros Barreto, Universidade Federal do Pará , Rua dos Mundurucus, 4487, Bairro Guamá, CEP 66075-000, Belém, Pará, BrazilTel +5591993484649 Email edifalcao@ufpa.br

Karla Valéria Batista Lima Evandro Chagas Institute , Br 316, km 7, s/n., Ananindeua, Pará, BrazilTel +559132142116 Email karlalima@iec.pa.gov.br

Author information

Edilene do Socorro Nascimento Falcão Sarges http://orcid.org/0000-0002-6608-8856

Yan Corrêa Rodrigues http://orcid.org/0000-0002-9922-4797

Ismari Perini Furlaneto http://orcid.org/0000-0001-9941-0162

Marcos Vinicios Hino de Melo http://orcid.org/0000-0002-9589-2958

Kátia Cilene Machado Lopes http://orcid.org/0000-0002-2517-6104

Karla Valéria Batista Lima http://orcid.org/0000-0001-5807-0392

Article

Publisher ID: 273759

DOI: 10.2147/IDR.S273759

PMC ID: 7588269

PubMed ID: 33116695

SO-VID: a3278ec1-9492-4829-aa29-0bf6de97d4d7

License:

This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms ( https://www.dovepress.com/terms.php).

History

Date received : 24 July 2020

Date accepted : 25 August 2020

Page count

Figures: 0, Tables: 16, References: 37, Pages: 11

Funding

Funded by: Fundação de Amparo à Pesquisa do Pará/Universidade do Estado do Pará (FAPESPA/UEPA);

Funded by: Programa Institucional de Bolsas de Iniciação Científica/Fundação Amazônia Paraense de Amparo à Pesquisa/Universidade do Estado do Pará (FAPESPA/UEPA);

Funded by: Programa Institucional de Bolsas de Iniciação Científica/Instituto Evandro Chagas – Conselho Nacional de Desenvolvimento Científico e Tecnológico (PIBIC/IEC/CNPq);

Funded by: Instituto Evandro Chagas/Ministério da Saúde/Secretaria de Vigilância em Saúde (IEC/MS/SVS);

This research was supported by funding from Fundação de Amparo à Pesquisa do Pará/Universidade do Estado do Pará (FAPESPA/UEPA) [Cooperation grant Nº004/2019], Programa Institucional de Bolsas de Iniciação Científica/Fundação Amazônia Paraense de Amparo à Pesquisa/Universidade do Estado do Pará (FAPESPA/UEPA) [Cooperation grant Nº001/2017/PPGBPA], Programa Institucional de Bolsas de Iniciação Científica/Fundação Amazônia Paraense de Amparo à Pesquisa/Universidade do Estado do Pará (FAPESPA/UEPA) [Cooperation grant Nº002/2019/Graduação], Programa Institucional de Bolsas de Iniciação Científica/Instituto Evandro Chagas – Conselho Nacional de Desenvolvimento Científico e Tecnológico (PIBIC/IEC/CNPq) and Instituto Evandro Chagas/Ministério da Saúde/Secretaria de Vigilância em Saúde (IEC/MS/SVS).

Pseudomonas aeruginosa Type III Secretion System Virulotypes and Their Association with Clinical Features of Cystic Fibrosis Patients

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Abstract

Purpose

Materials and Methods

Results

Conclusion

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Most cited references 36

Cystic fibrosis.

Pseudomonas aeruginosa: new insights into pathogenesis and host defenses.

Prevalence of type III secretion genes in clinical and environmental isolates of Pseudomonas aeruginosa.

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