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Antibiotic resistant pathogen outbreak investigation: an interdisciplinary module to teach fundamentals of evolutionary biology.

ABSTRACT: The evolution of resistance to antibiotics provides a timely and relevant topic for teaching undergraduate students evolutionary biology. Here, we present a module incorporating modified sequencing data from eight antibiotic resistant pathogen outbreaks in hospital settings with bioinformatics and phylogenetic analyses. This module uses whole genome sequencing data from hospital outbreaks investigated by the Centers for Disease Control and Prevention to provide examples of antibiotic resistance spread. Students work in groups to analyze outbreak data to identify the bacterial species and antibiotic resistance genes, to infer a phylogenetic tree examining relatedness among isolates, and to determine a possible source of the outbreak. Students then compile their results in individual reports and provide recommendations for preventing the further spread of antibiotic resistant organisms. In addition to providing genomic outbreak data, we include a teaching concepts guide discussing three integral components of the module: how evolutionary biology concepts of natural selection and competition impact antibiotic resistance; outbreak investigation information to aid in phylogenetic analysis and creation of recommendations; and instructions for the bioinformatics protocol. Completion of this module provides students an opportunity to think critically about the evolution of resistance, practice bioinformatics techniques, and relate evolutionary biology to current events.

SUBMITTER: Pierce AA

PROVIDER: S-EPMC6502480 | biostudies-literature | 2019

REPOSITORIES: biostudies-literature

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Antibiotic resistant pathogen outbreak investigation: an interdisciplinary module to teach fundamentals of evolutionary biology.

Pierce Amanda A AA de Man Tom J B TJB

Journal of biological education 20180309 2

The evolution of resistance to antibiotics provides a timely and relevant topic for teaching undergraduate students evolutionary biology. Here, we present a module incorporating modified sequencing data from eight antibiotic resistant pathogen outbreaks in hospital settings with bioinformatics and phylogenetic analyses. This module uses whole genome sequencing data from hospital outbreaks investigated by the Centers for Disease Control and Prevention to provide examples of antibiotic resistance ...[more]

PMID: 31073246

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Project description:Outbreak investigations are essential to control and prevent the dissemination of pathogens. This study developed and validated a complete analysis protocol for faster and more accurate surveillance and outbreak investigations of antibiotic-resistant microbes based on Oxford Nanopore Technologies (ONT) DNA whole-genome sequencing. The protocol was developed using 42 methicillin-resistant Staphylococcus aureus (MRSA) isolates identified from former well-characterized outbreaks. The validation of the protocol was performed using Illumina technology (MiSeq, Illumina). Additionally, a real-time outbreak investigation of six clinical S. aureus isolates was conducted to test the ONT-based protocol. The suggested protocol includes: (1) a 20 h sequencing run; (2) identification of the sequence type (ST); (3) de novo genome assembly; (4) polishing of the draft genomes; and (5) phylogenetic analysis based on SNPs. After the sequencing run, it was possible to identify the ST in 2 h (20 min per isolate). Assemblies were achieved after 4 h (40 min per isolate) while the polishing was carried out in 7 min per isolate (42 min in total). The phylogenetic analysis took 0.6 h to confirm an outbreak. Overall, the developed protocol was able to at least discard an outbreak in 27 h (mean) after the bacterial identification and less than 33 h to confirm it. All these estimated times were calculated considering the average time for six MRSA isolates per sequencing run. During the real-time S. aureus outbreak investigation, the protocol was able to identify two outbreaks in less than 31 h. The suggested protocol enables identification of outbreaks in early stages using a portable and low-cost device along with a streamlined downstream analysis, therefore having the potential to be incorporated in routine surveillance analysis workflows. In addition, further analysis may include identification of virulence and antibiotic resistance genes for improved pathogen characterization.

Project description:We provide the first analysis and synthesis of the evolutionary and mechanistic bases for risk of endometriosis in humans, structured around Niko Tinbergen's four questions about phenotypes: phylogenetic history, development, mechanism and adaptive significance. Endometriosis, which is characterized by the proliferation of endometrial tissue outside of the uterus, has its phylogenetic roots in the evolution of three causally linked traits: (1) highly invasive placentation, (2) spontaneous rather than implantation-driven endometrial decidualization and (3) frequent extensive estrogen-driven endometrial proliferation and inflammation, followed by heavy menstrual bleeding. Endometriosis is potentiated by these traits and appears to be driven, proximately, by relatively low levels of prenatal and postnatal testosterone. Testosterone affects the developing hypothalamic-pituitary-ovarian (HPO) axis, and at low levels, it can result in an altered trajectory of reproductive and physiological phenotypes that in extreme cases can mediate the symptoms of endometriosis. Polycystic ovary syndrome, by contrast, is known from previous work to be caused primarily by high prenatal and postnatal testosterone, and it demonstrates a set of phenotypes opposite to those found in endometriosis. The hypothesis that endometriosis risk is driven by low prenatal testosterone, and involves extreme expression of some reproductive phenotypes, is supported by a suite of evidence from genetics, development, endocrinology, morphology and life history. The hypothesis also provides insights into why these two diametric, fitness-reducing disorders are maintained at such high frequencies in human populations. Finally, the hypotheses described and evaluated here lead to numerous testable predictions and have direct implications for the treatment and study of endometriosis. Lay summary: Endometriosis is caused by endometrial tissue outside of the uterus. We explain why and how humans are vulnerable to this disease, and new perspectives on understanding and treating it. Endometriosis shows evidence of being caused in part by relatively low testosterone during fetal development, that 'programs' female reproductive development. By contrast, polycystic ovary syndrome is associated with relatively high testosterone in prenatal development. These two disorders can thus be seen as 'opposite' to one another in their major causes and correlates. Important new insights regarding diagnosis, study and treatment of endometriosis follow from these considerations.

Dataset Information

Antibiotic resistant pathogen outbreak investigation: an interdisciplinary module to teach fundamentals of evolutionary biology.

Publications

Antibiotic resistant pathogen outbreak investigation: an interdisciplinary module to teach fundamentals of evolutionary biology.

Similar Datasets

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