Experimental Bacterial Endocarditis in the Opossum (Didelphis virginiana).

Vakilzadeh, J; Rowlands, David T.; Sherwood, B. F.; LeMay, J. C.

doi:10.1093/infdis/122.1-2.89

Cited by 13 publications

(4 citation statements)

References 7 publications

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“…followed by bacterial colonization of the nascent thrombus (Keynan and Rubinstein, 2013). Close review of the historical, pre-1975 literature, however, reveals that IE has been reported in numerous, diverse animal models without this damage (Wadsworth, 1919;Jones, 1969;Vakilzadeh et al, 1970;Jones, 1972). In particular, authors specifically note that, while pre-infection mechanical ablation of the endothelium increases the rates of vegetation formation (and thus decreases the number of animals needed for a given set of experiments), this is a function of efficiency and convenience, not a biological requirement (Durack and Beeson, 1972a;Durack and Beeson, 1972b;Durack et al, 1973).…”

Section: Discussionmentioning

confidence: 99%

Enterococcal Endocarditis: Hiding in Plain Sight

Barnes

Frank

Dunny

2021

Front. Cell. Infect. Microbiol.

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Enterococcus faecalis is a major opportunistic bacterial pathogen of increasing clinical relevance. A substantial body of experimental evidence suggests that early biofilm formation plays a critical role in these infections, as well as in colonization and persistence in the GI tract as a commensal member of the microbiome in most terrestrial animals. Animal models of experimental endocarditis generally involve inducing mechanical valve damage by cardiac catheterization prior to infection, and it has long been presumed that endocarditis vegetation formation resulting from bacterial attachment to the endocardial endothelium requires some pre-existing tissue damage. Here we review both historical and contemporary animal model studies demonstrating the robust ability of E. faecalis to directly attach and form stable microcolony biofilms encased within a bacterially-derived extracellular matrix on the undamaged endovascular endothelial surface. We also discuss the morphological similarities when these biofilms form on other host tissues, including when E. faecalis colonizes the GI epithelium as a commensal member of the normal vertebrate microbiome - hiding in plain sight where it can serve as a source for systemic infection via translocation. We propose that these phenotypes may allow the organism to persist as an undetected infection in asymptomatic individuals and thus provide an infectious reservoir for later clinical endocarditis.

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Section: Discussionmentioning

confidence: 99%

Enterococcal Endocarditis: Hiding in Plain Sight

Barnes

Frank

Dunny

2021

Front. Cell. Infect. Microbiol.

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“…Most current frameworks assume an initial host immune reaction involving platelets, soluble components of the coagulation cascade, etc., with subsequent bacterial invasion of the emerging thrombus [ 158 , 159 ]. Upon close scrutiny of the historical references prior to 1975, however, IE has been described in a wide variety of animal experimental settings in the absence of such damage [ 160 , 161 , 162 , 163 , 164 , 165 ]. The researchers found that removing the endothelium prior to infection increased the rate of vegetation formation and reduced the number of animals required for the experiments.…”

Section: Point and Counterpointmentioning

confidence: 99%

Current Knowledge of Enterococcal Endocarditis: A Disease Lurking in Plain Sight of Health Providers

Nappi

2024

Pathogens

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Enterococcus faecalis is a bacterial pathogen that can cause opportunistic infections. Studies indicate that initial biofilm formation plays a crucial regulatory role in these infections, as well as in colonising and maintaining the gastrointestinal tract as a commensal member of the microbiome of most land animals. It has long been thought that vegetation of endocarditis resulting from bacterial attachment to the endocardial endothelium requires some pre-existing tissue damage, and in animal models of experimental endocarditis, mechanical valve damage is typically induced by cardiac catheterisation preceding infection. This section reviews historical and contemporary animal model studies that demonstrate the ability of E. faecalis to colonise the undamaged endovascular endothelial surface directly and produce robust microcolony biofilms encapsulated within a bacterially derived extracellular matrix. This report reviews both previous and current animal model studies demonstrating the resilient capacity of E. faecalis to colonise the undamaged endovascular endothelial surface directly and produce robust microcolony biofilms encapsulated in a bacterially derived extracellular matrix. The article also considers the morphological similarities when these biofilms develop on different host sites, such as when E. faecalis colonises the gastrointestinal epithelium as a commensal member of the common vertebrate microbiome, lurking in plain sight and transmitting systemic infection. These phenotypes may enable the organism to survive as an unrecognised infection in asymptomatic subjects, providing an infectious resource for subsequent clinical process of endocarditis.

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“…Several factors are important to the pathogenesis of IE, such as a fully functional immune system and clotting cascade as well as flow conditions within the heart, are difficult to replicate in vitro and thus, in many cases findings should be confirmed using in vivo IE models. IE has been induced in mice ( Liesenborghs et al, 2019 ; Schwarz et al, 2021 ), rats ( Heraief et al, 1982 ; Xiong et al, 2005 ; Veloso et al, 2011 ; Augustin et al, 2013 ), rabbits ( Durack et al, 1973 ; Crosby et al, 2016 ), pigs ( Johnson et al, 1986 ; Christiansen et al, 2013 ), dogs ( Highman et al, 1956 ), horses ( Else and Holmes, 1972 ) and opossums ( Vakilzadeh et al, 1970 ). In vivo IE models have been extensively used for wide-ranging research questions from pathogenesis to treatment outcomes ( Lerche et al, 2021 ).…”

Section: Investigative Research Approachesmentioning

confidence: 99%

Native valve, prosthetic valve, and cardiac device-related infective endocarditis: A review and update on current innovative diagnostic and therapeutic strategies

Kouijzer

Noordermeer²,

Leeuwen³

et al. 2022

Front. Cell Dev. Biol.

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Infective endocarditis (IE) is a life-threatening microbial infection of native and prosthetic heart valves, endocardial surface, and/or indwelling cardiac device. Prevalence of IE is increasing and mortality has not significantly improved despite technological advances. This review provides an updated overview using recent literature on the clinical presentation, diagnosis, imaging, causative pathogens, treatment, and outcomes in native valve, prosthetic valve, and cardiac device-related IE. In addition, the experimental approaches used in IE research to improve the understanding of disease mechanisms and the current diagnostic pipelines are discussed, as well as potential innovative diagnostic and therapeutic strategies. This will ultimately help towards deriving better diagnostic tools and treatments to improve IE patient outcomes.

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Experimental Bacterial Endocarditis in the Opossum (Didelphis virginiana).

Cited by 13 publications

References 7 publications

Enterococcal Endocarditis: Hiding in Plain Sight

Enterococcal Endocarditis: Hiding in Plain Sight

Current Knowledge of Enterococcal Endocarditis: A Disease Lurking in Plain Sight of Health Providers

Native valve, prosthetic valve, and cardiac device-related infective endocarditis: A review and update on current innovative diagnostic and therapeutic strategies

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