Isolation and Chemical Composition of Dinoflagellate Nuclei*

Nuclei were isolated from Peridinium cinctum. Peridinium trochoideum, Gyrodinium cohnii (Cryptothecodinium cohnii) and Gymnodinium nelsoni. The nuclei of G. cohnii, P. trochoideum and G. nelsoni were found to contain ～ 6.9, 34 and 143 picograms of DNA respectively. The ratios to DNA of RNA, acid-soluble and acid-insoluble protein for G. cohnii were 0.32, 0.13 and 0.99, respectively. The corresponding values for P. trochoideum were 0.22, 0.08 and 1.22, while those for G. nelsoni were 0.21, 0.10 and 1.09. The chemical composition of dinoflagellate nuclei is compared and contrasted with that of typical eukaryotic nuclei. The culture of these difficult organisms also is discussed.     

海产贝类尼氏单抱子虫病害的研究进展

目前,我国形成规模养殖的经济贝类有近20种,贝类增养殖已经成为沿海海水养殖业的支柱产业。资料显示,2004年全国海水贝类产量为1024万吨,占海水养殖总产量的77．82％。但是目前,由于气候变化、海洋环境污染、外来生物入侵等因素导致我国海产贝类病害越来越重,寄生虫就是主要病原之一,其中尼氏单孢子虫就是其中的一种原生动物寄生虫,寄生于很多种海产贝类体内。这种病害在很多地区都有暴发,国外对其研究较多,国内梁玉波等时这一病害进行了研究。因此,系统阐述国外贝类尼氏单孢子虫病害的研究现状与进展,对我国海产贝类病害的研究具有现实意义。本文时尼氏单孢子虫的分类、病害的流行情况、尼氏单孢子虫的形态学,病害的主要症状。尼氏单孢子虫的检测方法,尼氏单孢子虫与寄主之间的交互作用,环境因素时病害流行的影响等方面进行了论述,为我国贝类病害的研究和防治提供参考。     

The Citreoline Trogon as an Ecosystem Engineer1

The western Mexican endemic Citreoline Trogon (Trogon citreolus) builds its nest cavities in arboreal termitaria. We studied the reuse of these holes by other organisms after the trogons abandoned them in the tropical dry forest of western Mexico. Of the 24 cavities examined, 19 were occupied (5 by mammals and 14 by arthropods). We found two western Mexico endemic mammals (Marmosa canescens and Xenomys nelsoni) using these spaces. Our results suggest that the T. citreolus provides a critical role in creating necessary cavities for many organisms in tropical dry forests.     

A PCR-ELISA Method for Direct Detection of the Oyster Pathogen Haplosporidium nelsoni

A rapid method, utilizing both polymerase chain reaction (PCR) and enzyme-linked immunosorbent assay (ELISA), was developed for detection of oyster MSX disease. The technique included using Haplosporidium nelsoni pathogen-specific PCR primers (based on ribosomal RNA genes), a Chelex resin (for rapid DNA extraction from oyster mantle tissues), and cloned H. nelsoni rRNA plasmid DNA (for use as a capture probe). Digoxigenin was incorporated into the pathogen-specific PCR products, which were captured by the coated probe in a fast hybridization reaction and then detected by ELISA. The sensitivity of PCR amplification on cloned plasmid DNA was 10 fg for detection by stained agarose gel, and increased to 0.01 fg for ELISA. Positive signals were observed in infected oysters using the PCR-ELISA technique. This method may be applicable to early detection of infection. Received April 14, 1998; accepted September 30, 1998.     

Epizootic and Enzootic Aspects of Minchinia nelsoni (Haplosporida) Disease in Maryland Oysters

SYNOPSIS. Minchinia nelsoni disease in oysters (Crassostrea virginica) from Marumsco Bar, Pocomoke Sound, Maryland (an estuarine tributary of Chesapeake Bay) was studied for 8 years (1961–68) to determine epizootiologic relationships concerning life cycle of the parasite, pathologic effects on the host, and effects of physical factors on population density and recruitment of the host and parasite. The study period covered pre-epizootic, epizootic, and post-epizootic disease conditions. Data on the native oyster population as well as annual introductions of previously unexposed, susceptible populations of juvenile oysters from 1965–68 were included. Salinity, water temperature, mortality, prevalence, incidence, life cycle stages, gross pathology, and histopathologic relationships were observed. Mortality was high (45–55% per year) during the first 3 years of the study; however, M. nelsoni prevalences were low (> 25%) and did not clearly imply a cause and effect relationship. Drought conditions that began in the summer of 1963 and continued through 1967 caused higher salinities, and apparently initiated epizootic disease in the native oyster population. The epizootic peaked in May 1965 with a diagnosed prevalence in native oysters of 70%. Enzootic levels of annual mortality (40% in 1966, 30% in 1967, and 2% in 1968) and fall prevalence (16%, 24%, and 4%) developed after that time. Introduced populations had a typical epizootiologic pattern in 1965 (55% annual mortality, 82% incidence) and 1966 (55% annual mortality, 66% incidence) which declined in 1967 (30% annual mortality, 44% incidence) followed by a disappearance of the disease in 1968. Epizootiologic differences noted between native oysters (adult and juvenile) and the introduced juvenile populations were also evident from the stages of the disease. Infections in native animals tended to be less serious, and in many cases were delayed or attenuated, while infections in introduced oysters progressed to advanced or terminal phases. Occult manifestations (mantle recession thought to be due to M. nelsoni in oysters not showing histologic evidence of infection) were absent in introduced populations and common in the native population. These differences are interpreted as evidence of resistance in surviving native oysters and their progeny, and may indicate genetic resistance developed by natural selection and manifested by an increased ability to survive and overcome infection.