Equine herpesvirus abortion in Australia 1977 to 1982

Until 1977 no case of abortion caused by equine herpesvirus 1 (EHV1) had been recorded in Australia although the virus, called equine rhinopneumonitis virus, had been known to have been present at least since 1962. Outbreaks of EHV1 abortion occurred in New South Wales in 1977 and in 1981. Sporadic cases of EHV1 abortion had been confirmed in some parts of Australia each year since 1975. It was concluded that an abortigenic subtype of EHV1 had been introduced to Australia in 1977 and that the previously endemic respiratory subtype occasionally caused abortion. Virus isolation in a variety of cell cultures and histopathological examination of tissue were shown to be satisfactory methods of diagnosis of EHV1 abortion. Lung proved to be the specimen of choice. Slight serological differences between "abortigenic" and "respiratory" subtypes of EHV1 were found in cross neutralisation tests. A serological survey of 219 Sydney horses of various ages revealed that most yearlings had already acquired neutralising antibody to both subtypes.     

Experimental transmission of intestinal coccidiosis to piglets: clinical, parasitological and pathological findings.

Twenty-eight piglets coming from a "specific pathogen free" herd were inoculated at three days of age with 50 000 or 100 000 sporulated oocysts of Isospora suis. Fecal samples were examined for oocyst shedding daily and several clinical parameters were recorded. Ten piglets were used as normal controls. Groups of piglets were euthanized from three days to 12 days postinoculation and routine necropsies were performed. Bacteriological, virological, parasitological and histopathological examinations were made on the intestinal tracts. The incubation period was four to five days. Clinical signs and microscopic intestinal lesions observed in the experimentally infected animals were similar to those reported in spontaneous cases of porcine neonatal coccidiosis. Lesions of villous atrophy in the small intestine seemed to result from the destruction of villous epithelial cells mainly during the peak of asexual reproduction which occurred around four to five days postinoculation. Intracellular coccidial organisms were difficult to find during the late atrophic and villous regrowth stages of the intestinal lesions. The prepatent period varied from four to seven days and the most common was five days. Eighty percent of the piglets kept alive more than four days postinoculation have shed oocysts. Piglets dosed with old sporulated oocysts (ten months old) shed many more oocysts than those infected with a fresh inoculum (less than two months old). The patent period was not determined precisely with the design of the experiment but some of the infected piglets shed oocysts for at least five days.     

Further characterization of dandelion yellow mosaic virus from lettuce and dandelion

A damaging virus isolated in the Netherlands from lettuce was studied and compared with a virus isolated from dandelion orginating from Czechoslovakia. It was found to biologically resemble dandelion yellow mosaic virus incompletely described from dandelion and lettuce in Great Britain (Kassanis, 1944, 1947) and from dandelion in Germany (Hein, 1963). Mechanical transmission was greatly improved by buffer solution and transmission byMyzus persicae seemed to be in the non-persistent manner. Longevity in vitro of the virus hardly exceeded one day. Thermal inactivation was between 60 and 65 °C and the dilution end-point was between 10 000 and 100 000. It was still infectious in leaf material dried and stored over CaCl₂ at 4 °C for 6 1/2 years. The virus was isolated and purified with difficulty and was found to consist of one type of spherical particle of ca 30 nm diameter, with a sedimentation coefficient of 159 S, a buoyant density of 1.42 g.cm^?3 and an A₂₆₀/A₂₈₀ ratio of 1.67. An antiserum was prepared with a titre of 256 in the agar double-diffusion test. The virus could be identified in crude extracts from lettuce andChenopodium amaranticolor by enzyme-linked immunosorbent assay (ELISA), but not by agar double diffusion. It could only be visualized in crude sap in the electron microscope after trapping of virus particles on antiserum-coated grids. The virus cannot yet be assigned to any known virus group. It is of potential economic importance to lettuce because of its occurrence in widely differing regions in Europe, its aggressiveness and virulence on 22 out of 23 lettuce cultivars tested (and on endive) and its pathogenicity toLactuca genotypes which are resistant to lettuce mosaic virus and other important pathogens of lettuce. ‘Laibacher Eis’ was the only cultivar showing some tolerance.     

The genetic control of antibody formation

Studies of the molecular biology of lymphoid cells have markedly increased our understanding of how millions of different antibodies can be synthesized by a single animal. To date, the most detailed understanding has been achieved for the mouse, primarily because of the relatively greater experimental availability of this species. These studies, as well as those involving other species, have shown that the complete genes for antibody polypeptide chains are assembled from disparate genetic elements which are originally widely separated in the genome. The assembly process itself, together with the coding information present in the germ line genetic elements, contributes to the diversity of structure (and thus combining specificities) shown by mature antibody molecules. Specifically, the diversity of structure characteristic of antibody variable regions is due to three distinct mechanisms: innate variability of germ line genes; mismatching of individual gene segments during their somatic rearrangement leading to junctional diversity; and somatic mutation in variable region genetic material during or after the rearrangement. These processes lead to the wide array of combining specificities that permit the humoral immune system of a mature animal to interact with essentially any non-self antigen which it encounters. Complex genetic rearrangements are also responsible for the class switching phenomenon long known to be characteristic of the humoral immune response. A form of homologous recombination between constant region genes, possibly mediated by specific "switching" enzymes, is now believed to be involved in this phenomenon. It is also currently believed that the restriction of gene rearrangement processes to one of the two possible chromosomes of a diploid pair in each cell is responsible for the phenomenon of allelic exclusion that has long been associated with the normal functioning of mammalian B-cells.