The phylogenetic relationship to a free-living sister group, acanthocephalans are attractive candidates as model organisms for studying host-parasite co-evolution. For example, the species distribution within the host illustrates that fish and birds are the most widely used definitive hosts, followed by mammals. It is, however, interesting to note that the oldest group of vertebrates, the fish, is not utilized by significantly more species than the youngest groups, the birds and mammals, indicating expansive adaptive radiation in these newly explored host groups. We are aware that the presented molecular phylogeny of the Acanthocephala is not yet comprehensive, and needs to be tested and validated by future studies. This requires further taxon sampling and ideally the inclusion of additional molecular markers. However, our data also demonstrate the preliminary nature of the acanthocephalan classification in general, especially of the derived echinorhynchids, the most common acanthocephalans in fish.
We suggest that the current state of knowledge warrants the identification of further morphological characters for a better understanding of the acanthocephalan diversity, perhaps best driven by more in-depth molecular phylogenetic studies. This will enable the mapping of more morphological characters onto the molecular trees, and redefining the higher level classification of the Acanthocephala. Acanthocephalans are attractive candidates as model organisms for studying the ecology and co-evolutionary history of parasitic life cycles in the marine ecosystem. However, the lack of phylogenetic studies and taxonomic identification of especially marine Acanthocephala prevents detailed comparison to other endoparasites. We do hope that our study will iniciate future research on the species composition, zoogeography and evolution of the phylum Acanthocephala, allowing comparisons to be made on the ecology of this taxon and other species groups such as the nematodes and cestodes that have diversified under similar conditions. The conversion of NADP+ to NADPH by G6PD is the ratelimiting reaction in the pentose phosphate pathway, the primary source of reducing potential for the glutathione redox flux which serves to as the primary protection of erythrocytes against oxidative stress.
Numerous drugs and chemicals such as primaquine, foods or stress can induce hemolytic anemia in G6PD-deficient individuals. G6PD deficiency is the Olaparib second most common hereditary enzyme deficiency which affects approximately 400 million people worldwide and is distributed in areas of current and previous endemic malaria. This human enzyme defect is caused by mutations in the G6PD gene located on chromosome Xq28; thus, transmission of the genetic defect is X linked. Hemizygote males are most affected and homozygous females least affected; both are prone to red cell haemolysis. Heterozygote females have mixed G6PD normal and deficient red cells and their susceptibility to haemolysis depends on the balance between the expression of the normal and abnormal X chromosomes.