Feeder fish is the generic name for certain types of inexpensive fish commonly fed as live prey to captive animals such as sharks, turtles and some other fish such as oscars.
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To image and understand host-fungus interactions in the context of a live host, we developed the zebrafish larva as a transparent vertebrate model of disseminated candidiasis. We show that this infection faithfully reproduces many aspects of candidemia in mammalian hosts, with C. albicans disseminating throughout the host, proliferating, and killing the host. We describe the consequences of phagocytosis of C. albicans in the intact host and describe how this event can lead to a temporary impasse in which neither host cells nor fungi perish immediately. We also demonstrate that the activities of fungal and host factors are conserved in this infection model, including a dependence on fungal hyphal growth for virulence and a host requirement of NADPH oxidase for resistance to infection. Finally, we exploited the power of this model to noninvasively visualize the cellular impact of the loss of NADPH oxidase activity. We found that the host NADPH oxidase is the major cause of oxidative stress in C. albicans during infection and is of vital importance in both limiting fungal proliferation and limiting filamentous growth.
Here's a look at amazing images of the oddball fish.
The zebrafish larva is a unique and powerful model for noninvasively visualizing and understanding the interactions of pathogens with the innate immune system (, , ). Notably, zebrafish have similar signaling through Toll-like receptors to that in humans, express similar cytokines, and have macrophages, neutrophils, dendritic cells, mast cells, eosinophils, T cells, and B cells (). The delayed development of T cells and B cells, which do not mature until approximately 30 days postfertilization, permits a natural focus on innate immunity in embryonic and larval infection models. A larval model of candidemia offers several advantages compared to other recently described models of zebrafish infection with C. albicans. Specifically, the adult zebrafish candidemia model does not permit real-time visualization of infection or morpholino (MO)-directed gene knockdown, both of which are techniques available with the larval host (). Also, while others have described a localized embryonic zebrafish infection model (), it is not clear if and how these infections parallel human diseases of clinical importance, such as disseminated candidiasis. A larval zebrafish model of disseminated candidiasis offers a clinically relevant disease in a transparent and small host that relies on innate immunity and can be perturbed by antisense morpholino-mediated gene knockdown (, , ). These advantages have been exploited by others to identify novel immune mediators of infectious disease (, ) and provide a unique opportunity to address the molecular nature of in vivo interactions between C. albicans and immune cells in the context of a live host.
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