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Biology subjects

Papke, E.

Publications and source records attributed to Papke, E..

3 recordsLinked to original sources

Temperate and filamentous bacteriophages as reservoirs of bacterial virulence in stony coral tissue loss disease

Lysogenic conversion, in which bacteriophages (viruses that infect bacteria) integrate into bacterial genomes and confer new phenotypic traits on their hosts, is a well-established mechanism for the emergence of pathogens. While this process underpins many bacterial diseases in humans and other animals, its role in coral disease remains largely unexplored. Here, we investigate the potential role of lysogenic conversion in stony coral tissue loss disease (SCTLD), which has caused unprecedented mortality of Caribbean corals since 2014 and for which the etiological agent remains unknown. Across 27 original coral samples and 178 publicly available metagenomes from the Florida Reef Tract spanning seven coral species, we detected a greater number of unique viral genomes capable of lysogeny in diseased corals or visually healthy portions of diseased corals (DD and HD, respectively) compared to visually healthy (VH) corals. SCTLD-associated bacteriophages were primarily predicted to infect bacterial taxa previously implicated in the disease, such as Vibrionales, Rhodobacterales, and Flavobacteriia, and carried abundant and widespread virulence genes with the potential to enhance bacterial colonization, competition, or direct host damage, including homologs of Tse2, Zot, RTX, pneumolysin, and cytolytic delta-endotoxin. Although causal relationships remain unresolved, our findings indicate that phages capable of lysogenic conversion have the genomic capacity to laterally transfer bacterial virulence genes in SCTLD-affected corals. The acquisition of genes via lysogenic conversion could contribute to bacterial virulence while maintaining community taxonomic profiles, helping to explain previous community profiling observations and providing a mechanistic framework for disease pathogenesis.

genomics↗

Multidisciplinary assessments of a potentially novel acute tissue loss disease on Florida Orbicella corals

Coral disease outbreaks are an increasingly common threat to reefs. While coral disease research is expanding rapidly, there are still monumental challenges in diagnosing and differentiating among the different diseases on a reef. We used a collaborative multidisciplinary approach to characterize a potentially novel disease affecting Orbicella faveolata colonies in the Florida Keys. We tagged and fate-tracked individual lesions for progression and cessation rates, reanalyzed in situ photographs of previously monitored corals to determine prevalence and seasonality, and assessed the efficacy of amoxicillin treatments. Samples collected from lesions as well as unaffected and healthy controls were used to examine microbiomes, assess nine coral pathological parameters via histology, and measure 19 symbiont-specific physiological metrics using transmission electron microscopy (TEM). Across all analyses, we concluded that the observed disease is unlikely to be SCTLD. Many, but not all, metrics had similarities to previous descriptions of white plague, and so we additionally conducted preliminary histology on presumed white plague samples of O. franksi for comparison. However, the dearth of quantifiable histology and TEM studies on white plague did not allow us to conclusively confirm or refute comparisons to white plague. Using the recommended coral disease nomenclature, we define this specific outbreak as "Orbicella acute tissue loss disease" (OATLD). We provide unprecedented, quantified descriptions across numerous metrics of both diseased and control colonies. We suggest that these data lay the groundwork for future efforts on this disease as well as a comprehensive set of parameters against which other diseases can be compared.

physiology↗

In vivo evolution of a Klebsiella pneumoniae capsule defect promotes complement-mediated opsono-phagocytosis and persistence during recurrent infection

Klebsiella pneumoniae carbapenemase-producing K. pneumoniae (KPC-Kp) bloodstream infections rarely overwhelm the host but are associated with high mortality. The complement system is a key host defense against bloodstream infection. However, there are varying reports of serum resistance among KPC-Kp isolates. We assessed growth of 59 KPC-Kp clinical isolates in human serum and found increased resistance in 16/59 (27%). We identified five genetically-related bloodstream isolates with varying serum resistance profiles collected from a single patient during an extended hospitalization marked by recurrent KPC-Kp bloodstream infections. We noted a loss-of-function mutation in the capsule biosynthesis gene, wcaJ, that emerged during infection was associated with decreased polysaccharide capsule content, and resistance to complement-mediated killing. Surprisingly, disruption of wcaJ increased deposition of complement proteins on the microbial surface compared to the wild-type strain and led to increased complement-mediated opsono-phagocytosis in human whole blood. Disabling opsono-phagocytosis in the airspaces of mice impaired in vivo control of the wcaJ loss-of-function mutant in an acute lung infection model. These findings describe the rise of a capsular mutation that promotes KPC-Kp persistence within the host by enabling co-existence of increased bloodstream fitness and reduced tissue virulence. O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=124 SRC="FIGDIR/small/542722v1_ufig1.gif" ALT="Figure 1"> View larger version (31K): org.highwire.dtl.DTLVardef@155736eorg.highwire.dtl.DTLVardef@10d47c0org.highwire.dtl.DTLVardef@e1ab83org.highwire.dtl.DTLVardef@1c33131_HPS_FORMAT_FIGEXP M_FIG Graphical abstract Created with BioRender.com C_FIG

microbiology↗