Zebrafish and Frog Models of <i>Mycobacterium marinum</i> Infection

Cosma, Christine L.; Swaim, Laura E.; Volkman, Hannah E.; Ramakrishnan, Lalita; Davis, J. Muse

doi:10.1002/0471729256.mc10b02s3

Cited by 71 publications

(77 citation statements)

References 22 publications

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“…The relatively rapidly growing human and animal pathogen Mycobacterium marinum, a close genetic relative of M. tuberculosis (49), is used to study the pathogenesis of tuberculosis (11,14,39,46,55). M. marinum causes systemic granulomatous infections and disease in its natural hosts, ectotherms such as fish and frogs, and peripheral chronic granulomatous disease (fish tank granulomas) in humans (10,11,19).…”

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“…M. marinum causes systemic granulomatous infections and disease in its natural hosts, ectotherms such as fish and frogs, and peripheral chronic granulomatous disease (fish tank granulomas) in humans (10,11,19). Inoculation of the leopard frog produces a long-term, asymptomatic infection with well-defined, nonnecrotizing granulomas that harbor bacteria (5,41).…”

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confidence: 99%

“…Inoculation of the leopard frog produces a long-term, asymptomatic infection with well-defined, nonnecrotizing granulomas that harbor bacteria (5,41). In contrast, experimental inoculation of goldfish, zebrafish, striped bass, or medaka produces necrotizing granulomas and ultimately lethal disease (7,11,12,24,39,40,48,53,54,59).…”

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confidence: 99%

“…Chemical and drug screens are also easily performed using this organism (37,38). Zebrafish become infected with M. marinum in fish facilities (57) and also develop disease upon experimental inoculation (11,12,22,23,40,54). A zebrafish embryo model of infection has been used to characterize the earliest events following mycobacterial infection in which macrophage aggregates with key features of tuberculous granulomas form (18).…”

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Mycobacterium marinum Infection of Adult Zebrafish Causes Caseating Granulomatous Tuberculosis and Is Moderated by Adaptive Immunity

Swaim¹,

Connolly²,

et al. 2006

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The zebrafish, a genetically tractable model vertebrate, is naturally susceptible to tuberculosis caused by Mycobacterium marinum, a close genetic relative of the causative agent of human tuberculosis, Mycobacterium tuberculosis. We previously developed a zebrafish embryo-M. marinum infection model to study host-pathogen interactions in the context of innate immunity. Here, we have constructed a flowthrough fish facility for the large-scale longitudinal study of M. marinum-induced tuberculosis in adult zebrafish where both innate and adaptive immunity are operant. We find that zebrafish are exquisitely susceptible to M. marinum strain M. Intraperitoneal injection of five organisms produces persistent granulomatous tuberculosis, while the injection of ϳ9,000 organisms leads to acute, fulminant disease. Bacterial burden, extent of disease, pathology, and host mortality progress in a time-and dose-dependent fashion. Zebrafish tuberculous granulomas undergo caseous necrosis, similar to human tuberculous granulomas. In contrast to mammalian tuberculous granulomas, zebrafish lesions contain few lymphocytes, calling into question the role of adaptive immunity in fish tuberculosis. However, like rag1 mutant mice infected with M. tuberculosis, we find that rag1 mutant zebrafish are hypersusceptible to M. marinum infection, demonstrating that the control of fish tuberculosis is dependent on adaptive immunity. We confirm the previous finding that M. marinum ⌬RD1 mutants are attenuated in adult zebrafish and extend this finding to show that ⌬RD1 predominantly produces nonnecrotizing, loose macrophage aggregates. This observation suggests that the macrophage aggregation defect associated with ⌬RD1 attenuation in zebrafish embryos is ongoing during adult infection.

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Mycobacterium marinum Infection of Adult Zebrafish Causes Caseating Granulomatous Tuberculosis and Is Moderated by Adaptive Immunity

Swaim¹,

Connolly²,

et al. 2006

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“…marinum causes disease in a large number of poikilothermic animals, including fish, frogs, and reptiles (6)(7)(8). The course of infection in these animals is highly similar to that of M. tuberculosis in the human host.…”

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Genome-Wide Transposon Mutagenesis Indicates that Mycobacterium marinum Customizes Its Virulence Mechanisms for Survival and Replication in Different Hosts

et al. 2015

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eThe interaction of environmental bacteria with unicellular eukaryotes is generally considered a major driving force for the evolution of intracellular pathogens, allowing them to survive and replicate in phagocytic cells of vertebrate hosts. To test this hypothesis on a genome-wide level, we determined for the intracellular pathogen Mycobacterium marinum whether it uses conserved strategies to exploit host cells from both protozoan and vertebrate origin. Using transposon-directed insertion site sequencing (TraDIS), we determined differences in genetic requirements for survival and replication in phagocytic cells of organisms from different kingdoms. In line with the general hypothesis, we identified a number of general virulence mechanisms, including the type VII protein secretion system ESX-1, biosynthesis of polyketide lipids, and utilization of sterols. However, we were also able to show that M. marinum contains an even larger set of host-specific virulence determinants, including proteins involved in the modification of surface glycolipids and, surprisingly, the auxiliary proteins of the ESX-1 system. Several of these factors were in fact counterproductive in other hosts. Therefore, M. marinum contains different sets of virulence factors that are tailored for specific hosts. Our data imply that although amoebae could function as a training ground for intracellular pathogens, they do not fully prepare pathogens for crossing species barriers.

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Adult Zebrafish Model of Streptococcal Infection

Phelps¹,

Runft

Neely

2009

CP Microbiology

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Streptococcal pathogens cause a wide array of clinical syndromes in humans, including invasive systemic infections resulting in high mortality rates. Many of these pathogens are human specific, and therefore difficult to analyze in vivo using typical animal models, as these models rarely replicate what is observed in human infections. This unit describes the use of the zebrafish (Danio rerio) as an animal model for streptococcal infection to analyze multiple disease states. This model closely mimics the necrotizing fasciitis/myositis pathology observed in humans from a Streptococcus pyogenes infection. The use of a zoonotic pathogen, Streptococcus iniae, which replicates systemic infections caused by many streptococcal pathogens, including dissemination to the brain, is also described. Protocols describing both intraperitoneal and intramuscular infections, as well as methods for histological and quantitative measurements of infection, are also described. Curr. Protoc. Microbiol. 13:9D.1.1–9D.1.27. © 2009 by John Wiley & Sons, Inc.

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Zebrafish and Frog Models of Mycobacterium marinum Infection

Cited by 71 publications

References 22 publications

Mycobacterium marinum Infection of Adult Zebrafish Causes Caseating Granulomatous Tuberculosis and Is Moderated by Adaptive Immunity

Mycobacterium marinum Infection of Adult Zebrafish Causes Caseating Granulomatous Tuberculosis and Is Moderated by Adaptive Immunity

Genome-Wide Transposon Mutagenesis Indicates that Mycobacterium marinum Customizes Its Virulence Mechanisms for Survival and Replication in Different Hosts

Adult Zebrafish Model of Streptococcal Infection

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