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been proposed that the same strategies which evolved over generations to evade phagocytic predation in amoebae have equipped bacteria for macrophage survival in the human body. For example, Legionella spp. can infect and kill both amoebae and macrophages, causing severe disease in human hosts. Moreover, Mycobacterium abscessus upregulates the secretion of the proteins that allow this bacterium to survive in a hostile environment and adapt to live intracellularly in FLA and consequently macrophages. Understanding how bacteria can survive within FLA can help dissect the pathogenesis of these bacterial infections. Conclusion The interactions between FLA and phagocyte-resistant bacteria present just one specific area in an almost endless supply of microbial interactions. Indeed, the interactions between amoebae and fungal or viral pathogens has not
to convert much quicker than is observed in the extracellular environment. For example, Aeromonas hydrophila has been shown to enter the VBNC form twenty days quicker within amoebae than it does alone; whilst in P. aeruginosa, the shift from the VBNC stage to the active state can occur in as little as two hours upon amoebic ingestion. Amoeba-driven VBNC conversion of bacteria is a fascinating by-product of their co- evolution and one that might prove to have significant clinical implications. Bacterial gymnasia: how amoebae alter the pathogenicity of bacteria Not only does the intimate relationship with amoebae protect bacteria from detection, disinfection and treatment, but it can also alter bacterial pathogenicity, allowing bacteria to become resistant to immune responses in their hosts. Amoebae and macrophages have similarities in phagocytosis. It has
78 Microbiology Today October 2022 | microbiologysociety.org
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