The most recent genome-editing system called CRISPR-Cas9 (clustered regularly interspaced short palindromic repeat system with associated protein 9-nuclease) was employed to delete four non-essential genes (i.e., Caeco1, Caidh1, Carom2, and Cataf10) individually to establish their gene functionality annotations in pathogen Candida albicans. The biological roles of these genes were investigated with respect to the cell wall integrity and biogenesis, calcium/calcineurin pathways, susceptibility of mutants towards temperature, drugs and salts. All the mutants showed increased vulnerability compared to the wild-type background strain towards the cell wall-perturbing agents, (antifungal) drugs and salts. All the mutants also exhibited repressed and defective hyphal growth and smaller colony size than control CA14. The cell cycle of all the mutants decreased enormously except for those with Carom2 deletion. The budding index and budding size also increased for all mutants with altered bud shape. The disposition of the mutants towards cell wall-perturbing enzymes disclosed lower survival and more rapid cell wall lysis events than in wild types. The pathogenicity and virulence of the mutants was checked by adhesion assay, and strains lacking rom2 and eco1 were found to possess the least adhesion capacity, which is synonymous to their decreased pathogenicity and virulence.
A new myxosporean species, Henneguya cynoscioni sp. n., is described from the spotted seatrout, Cynoscion nebulosus (Cuvier) (Sciaenidae) as a causative agent of cardiac henneguyosis. This new myxosporean species is characterized by the morphology of spores and the sequence of SSU rDNA. Examination of 227 spotted seatrout from four South Carolina estuaries in 2008-2010 revealed a 33.5% total prevalence of H. cynoscioni. Henneguya cynoscioni produces lesions in the bulbus arteriosus, its specific site of infection. The severity of lesions and their impact on the bulbus arteriosus is proportional to the number of plasmodial stages developing in this segment of the heart, being most pronounced in host reaction directed against spores liberated from plasmodia.
The original description of Myxobolus longisporus Nie et Li, 1992, the species infecting gills of Cyprinus carpio haematopterus L., is supplemented with new data on the spore morphology and pathogenicity. Spores are elongate pyriform with pointed anterior end, 15.7 (15.5-16.5) µm long, 6.7 (6-8) µm wide and 5.5 µm thick. Sutural ridge is straight and narrow. Mucus envelope is lacking. Two equal-sized elongate pyriform polar capsules are 8.5 µm long and 2.5 µm wide with convergent long axes. Polar filament coiled perpendicularly to the long axis of the capsule makes 9 (8-10) turns. Posterior end of polar capsules exceeds mid-spore by 15-20%. Cyst-like plasmodia are localised in the gill secondary lamellae. The infection is described in adult big host specimens. Gross lesions manifested as dark red colouration of gill tissues were restricted to the ventral part of the first gill arches. Remarkable site specificity (apical part of secondary lamellae) was observed in the course of development of microscopic lesions. M. longisporus is characterised also on the molecular level using sequences of SSU rRNA gene. Phylogenetic analysis based on these sequences has allowed clearer phylogenetic relationships to be established with other species of the genus Myxobolus sequenced to date.
During an ecological investigation of populations of the freshwater bryozoan, Cristatella mucedo Cuvier, parasitic sac-like stages of the myxozoan, Tetracapsula bryozoides Canning, Okamura et Curry, 1996 were discovered within the body cavity of some bryozoan colonies. Subsequent to their detection, data were collected on the incidence and prevalence of myxo-zoans in bryozoan populations in the Thames Valley region and on the effects of myxozoans on their hosts. Notable spatial and temporal variation in incidence and prevalence of myxozoans was documented. The production of statoblasts by bryozoans was significantly compromised by myxozoan infection although the production of larvae was not. Infection by myxozoans resulted in generalized swelling, malformation, degeneration, and slower response times in bryozoan colonies. These findings indicate that myxozoans adversely affect host fitness and may therefore influence population levels. Light microscopy revealed that multiple myxozoan sacs can be present within the continuous body cavity of bryozoan colonies and that sacs apparently undergo fission. Infective spores that develop within sacs are at least on some occasions released into the body cavity of bryozoans. Nothing is known of the subsequent stages in the life cycle of this myxozoan, including whether T. bryozoides infects another species. Spores may be released into the water column to infect new hosts or they may be introduced to new hosts when infected bryozoans are ingested.