Evidence map›Paper›PMID 31295255›Full record

ArticlePLoS computational biology2019

Identifying determinants of persistent MRSA bacteremia using mathematical modeling.

Tsuyoshi Mikkaichi, Michael R Yeaman, Alexander Hoffmann, MRSA Systems Immunobiology Group

Abstract read
In one paragraph

Article in PLoS computational biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

9 citing papers in PubMed.

  1. Computational and in vitro evaluation of probiotic treatments for nasalProceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  2. Review
  3. Treatment of MRSA Infection: Where are We?Current medicinal chemistry · 2024
    Review
  4. Review
  5. Article
  6. Review
  7. Review
  8. Article
  9. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors.

Tsuyoshi MikkaichiInstitute for Quantitative and Computational Biosciences, University of California, Los Angeles, California, United States of America.ORCID 0000-0002-8113-3408
Michael R YeamanDavid Geffen School of Medicine at UCLA, Los Angeles, California, United States of America.
Alexander HoffmannInstitute for Quantitative and Computational Biosciences, University of California, Los Angeles, California, United States of America.ORCID 0000-0002-5607-3845
MRSA Systems Immunobiology Group

Funding

Systems Immunolobiology of Antibiotic-Persistent MRSA InfectionU01AI124319 · NIAID · LUNDQUIST INSTITUTE FOR BIOMEDICAL INNOVATION AT HARBOR-UCLA MEDICAL CENTER · PI YEAMAN, MICHAEL R · 2016 to 2020
$10.1M
Mitigating Resistance & Virulence in MRSAR33AI111661 · NIAID · LUNDQUIST INSTITUTE FOR BIOMEDICAL INNOVATION AT HARBOR-UCLA MEDICAL CENTER · PI YEAMAN, MICHAEL R · 2016 to 2018
$1.2M
NIAID NIH HHS R33 AI111661NIAID NIH HHS U01 AI124319
6 · The paper itself

Abstract

Persistent bacteremia caused by Staphylococcus aureus (SA), especially methicillin-resistant SA (MRSA), is a significant cause of morbidity and mortality. Despite susceptibility phenotypes in vitro, persistent MRSA strains fail to clear with appropriate anti-MRSA therapy during bacteremia in vivo. Thus, identifying the factors that cause such MRSA persistence is of direct and urgent clinical relevance. To address the dynamics of MRSA persistence in the face of host immunity and typical antibiotic regimens, we developed a mathematical model based on the overarching assumption that phenotypic heterogeneity is a hallmark of MRSA persistence. First, we applied an ensemble modeling approach and obtained parameter sets that satisfied the condition of a minimum inoculum dose to establish infection. Second, by simulating with the selected parameter sets under vancomycin therapy which follows clinical practices, we distinguished the models resulting in resolving or persistent bacteremia, based on the total SA exceeding a detection limit after five days of treatment. Third, to find key determinants that discriminate resolving and persistent bacteremia, we applied a machine learning approach and found that the immune clearance rate of persister cells is a key feature. But, fourth, when relapsing bacteremia was considered, the growth rate of persister cells was also found to be a key feature. Finally, we explored pharmacological strategies for persistent and relapsing bacteremia and found that a persister killer, but not a persister formation inhibitor, could provide for an effective cure the persistent bacteremia. Thus, to develop better clinical solutions for MRSA persistence and relapse, our modeling results indicate that we need to better understand the pathogen-host interactions of persister MRSAs in vivo.

Indexed as

Anti-Bacterial AgentsBacteremiaFemaleHumansMaleMethicillin-Resistant Staphylococcus aureusMicrobial Sensitivity TestsModels, TheoreticalStaphylococcal InfectionsAnti-Bacterial Agents

Identifiers

PMID31295255
PMCPMC6622483

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.