Juvenile summer flounder, Paralichthys-dentatus, mortalities in the western Atlantic Ocean caused by the hemoflagellate Trypanoplasma bullocki : evidence from field and experimental studies

Juvenile summer flounder (140-200 mm) inoculated with T. bullocki by leech vector or syringe in November 1980, and held in flowing seawater tanks all died within 11 weeks. Water temperature during the period of highest mortality ranged from 0.5 to 1.5 °C and may have been a contributing factor in mortality. No uninoculated control fish died even though held in the same tank. Symptoms of disease were anemia, splenomegaly and obvious ascites. Mortality of feral juvenile summer flunder in the lower York River during January 1981 was also attributable to T. bullocki because of identical symptoms to moribund fish in the experiment. Results suggest that the presence of ascites can be used as an estimate of mortality in fishes north of Cape Hatteras

Some Histologic Gill Lesions of Several Estuarine Finfishes Related to Exposure to Contaminated Sediments: A Preliminary Report

Collections were made during 1983, \u2784 and \u2785 in the Elizabeth River, whose sediments are heavily contaminated with PAHs, heavy metals and other anthropogenic materials. Comparison samples were from the cleaner Nansemond River, another subestuary feeding into Hampton Roads (the lower James River) nearby. Most samples from all stations included three transient quasi-catadromous nektonic sciaenids, Atlantic croaker (Micropogonias undulatus), spot (Leiostomus xanthurus) and weakfish (Cynoscion regalis), and two endemic estuarine benthic fishes, hogchoker (Trinectes maculatus) and oyster toadfish (Opsanus tau).https://scholarworks.wm.edu/vimsbooks/1161/thumbnail.jp

The Hyperparasite, Urosporidium spisuli sp. n. (Haplosporea), and Its Effects on the Surf Clam Industry

SSurf clams (Spisula solidissima) from along the Virginia and North Carolina coasts are infected with an immature anisakid nematode worm which does not cause economic concern until infected with the protozoan hyperparasite, Urosporidium spisuli sp. n. When the protozoan sporulates the spores give the worm a brownish-black appearance, thus making it readily visible in clam tissues. Light and electron microscope studies of the spores reveal characteristics which differentiate the protozoan from other species of Urosporidium. All spores are killed after 5 to 30 min at 100 C; therefore, the consumer would not ingest live spores when eating commercially prepared clam meat

Bibliography of the Monogenetic Trematode Literature of the World, 1758 to 1969

In preparing this bibliography we have attempted to collect all literature references pertaining to the Monogenea. Accordingly it represents an up-to-date (through September 1969) guide to the literature of these parasites, and is of maximum scope, including not only taxonomic literature but also references to ecological and physiological studies on Monogenea as well as reports of preferred methods of treating infestations of these parasites

Skin ulcers in estuarine fishes: a comparative pathological evaluation of wild and laboratory-exposed fish.

The toxic dinoflagellate Pfiesteria piscicida Steidinger & Burkholder has recently been implicated as the etiologic agent of acute mass mortalities and skin ulcers in menhaden, Brevoortia tyrannus, and other fishes from mid-Atlantic U.S. estuaries. However, evidence for this association is largely circumstantial and controversial. We exposed tilapia (Oreochromis spp.) to Pfiesteria shumwayae Glasgow & Burkholder (identification based on scanning electron microscopy and molecular analyses) and compared the resulting pathology to the so-called Pfiesteria-specific lesions occurring in wild menhaden. The tilapia challenged by high concentrations (2,000-12,000 cells/mL) of P. shumwayaeexhibited loss of mucus coat and scales plus mild petecchial hemorrhage, but no deeply penetrating chronic ulcers like those in wild menhaden. Histologically, fish exhibited epidermal erosion with bacterial colonization but minimal associated inflammation. In moribund fish, loss of epidermis was widespread over large portions of the body. Similar erosion occurred in the mucosa lining the oral and branchial cavities. Gills exhibited epithelial lifting, loss of secondary lamellar structure, and infiltration by lymphoid cells. Epithelial lining of the lateral line canal (LLC) and olfactory organs exhibited severe necrosis. Visceral organs, kidney, and neural tissues (brain, spinal cord, ganglia, peripheral nerves) were histologically normal. An unexpected finding was the numerous P. shumwayae cells adhering to damaged skin, skin folds, scale pockets, LLC, and olfactory tissues. In contrast, histologic evaluation of skin ulcers in over 200 wild menhaden from Virginia and Maryland portions of the Chesapeake Bay and the Pamlico Estuary, North Carolina, revealed that all ulcers harbored a deeply invasive, highly pathogenic fungus now known to be Aphanomyces invadans. In menhaden the infection always elicited severe myonecrosis and intense granulomatous myositis. The consistent occurrence of this fungus and the nature and severity of the resulting inflammatory response indicate that these ulcers are chronic (age >1 week) and of an infectious etiology, not the direct result of an acute toxicosis initiated by Pfiesteria toxin(s) as recently hypothesized. The disease therefore is best called ulcerative mycosis (UM). This study indicates that the pathology of Pfiesteria laboratory exposure is fundamentally different from that of UM in menhaden; however, we cannot rule out Pfiesteria as one of many possible early initiators predisposing wild fishes to fungal infection in some circumstances

Stable interference of EWS–FLI1 in an Ewing sarcoma cell line impairs IGF-1/IGF-1R signalling and reveals TOPK as a new target

BACKGROUND: Ewing sarcoma is a paradigm of solid tumour -bearing chromosomal translocations resulting in fusion proteins that act as deregulated transcription factors. Ewing sarcoma translocations fuse the EWS gene with an ETS transcription factor, mainly FLI1. Most of the EWS–FLI1 target genes still remain unknown and many have been identified in heterologous model systems

Epigenetic targeting of Hedgehog pathway transcriptional output through BET bromodomain inhibition

Hedgehog signaling drives oncogenesis in several cancers and strategies targeting this pathway have been developed, most notably through inhibition of Smoothened. However, resistance to Smoothened inhibitors occurs via genetic changes of Smoothened or other downstream Hedgehog components. Here, we overcome these resistance mechanisms by modulating GLI transcription via inhibition of BET bromodomain proteins. We show the BET bromodomain protein, BRD4, regulates GLI transcription downstream of SMO and SUFU and chromatin immunoprecipitation studies reveal BRD4 directly occupies GLI1 and GLI2 promoters, with a substantial decrease in engagement of these sites upon treatment with JQ1, a small molecule inhibitor targeting BRD4. Globally, genes associated with medulloblastoma-specific GLI1 binding sites are downregulated in response to JQ1 treatment, supporting direct regulation of GLI activity by BRD4. Notably, patient- and GEMM-derived Hedgehog-driven tumors (basal cell carcinoma, medulloblastoma and atypical teratoid/rhabdoid tumor) respond to JQ1 even when harboring genetic lesions rendering them resistant to Smoothened antagonists

Host-parasite relationship of

Epithelial hyperplasia was the most distinctive pathological change in gill filaments of striped bass, Morone saxatilis (Walbaum), from the lower Chesapeake Bay infested by Ergasilus labracis Krøyer. This tissue reaction initiated in the filament area most adjacent to the mouth of the attached parasite. Interruption of parasite egg sac production and eventual dislodgement associated with swelling of the gill filaments occurred unilaterally on gill arches of either side of the branchial basket. The largest number of parasites in all fish was found on the first outer hemibranch while abundance on successive hemibranchs decreased in rank order. Copepods on the inner hemibranch, however, were least numerous on the first inner hemibranch and more numerous on the fourth inner hemibranch. On the whole, the number of parasites attached to the outer hemibranch outnumbered the number of parasites established on the inner hemibranchs. This differential settlement was most evident in low to moderate infections and became less apparent in heavy infections. Newly settled copepods showed highest abundance on the third arch and least abundance on the first and fourth arches. The causes for this differential distribution on the gill arches are discussed