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Microsporidia growth and host resistance in Nematocida-Caenorhabditis elegans interactions


The success of pathogens depends on their access to host space and resources. In addition to optimizing their use of the host environment, pathogens must evade host defenses. We investigated the growth dynamics of fungal-related obligate intracellular pathogens from the microsporidia group in the context of a whole animal host. Microsporidia infect virtually all animal phyla, but the details of their growth and interactions with the host are poorly characterized. We examined infections of the roundworm Caenorhabditis elegans by its natural microsporidian pathogens in the genus Nematocida. From these studies we have identified surprising pathogen growth strategies and constraints that limit this growth based on the host environment. Infection by just a single Nematocida parisii cell in a single host intestinal cell grows to fill the majority of the host organ before reaching the spore-formation stage of the life cycle. Microsporidia infections spread between neighboring host cells by inducing them to fuse into syncytia. Nematocida displodere infections caused syncytia formation in the muscle and epidermis, but not in the intestine. We also found that the decision to switch from replication to differentiation in N. parisii was altered by the density of infection, suggesting that environmental cues influence the dynamics of the pathogen life cycle. Additionally, we found that the success of N. parisii growth varies depending on the host environment. Specifically, we determined that host genotype and age could strongly affect the outcome of infection. In particular we found that a strain of C. elegans from Hawaii was resistant to N. parisii growth and could eliminate infection in an age-dependent manner, which is a trait with a complex genetic basis. Thus, we show how microsporidia can maximize the use of host space for growth, that environmental cues in the host can regulate a developmental switch in the pathogen, and that certain host environments can clear microsporidia infection. These findings advance our understanding of the selective pressures that can shape both host and microsporidia genomes over the course of their co-evolution.

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