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Summary The prevalence of antibodies to the EAM-1 strain of equine adenovirus was studied in six groups of horses, totalling 433, from New South Wales and Queensland, Australia, and New Zealand. Within groups, virus neutralising antibodies were detected in 69–100%, complement fixing antibodies in 41–68% and precipitating antibodies in 10–19%. The prevalence within areas was similar. Passive transfer of colostral antibodies to equine adenovirus from the mare to the foal was demonstrated. The prevalence of antibody to EAM-1 increased with age such that approximately 70% of yearlings and two-year-old horses possessed SN and CF antibodies; this incidence was similar to that of older horses.

Tyzzer's disease was diagnosed in a 17-day-old foal after the demonstration of multiple foci of hepatic necrosis and organisms morphologically compatible with Bacillus piliformis in hepatocytes at the margins of the necrotic foci. The bacilli were 300 to 500 nm in diameter with occasional giant bacilli 1000 nm in diameter. Many intranuclear organisms were seen, and an apparent sequence of nuclear penetration by these organisms was demonstrated. There was hemorrhage in the heart and inflammatory changes in the mesenteric lymph node. Enteritis was not present in the jejunum, which was the only portion of intestine available for examination.

During 1970 to 1972, 55 anestrous mares were used to study the therapeutic effect of daily oral applications of 40 to 60 mg chlormadinone acetate (CAP). Fourty animals received CAP, up to 18 (or 21) days, while 15 animals served as an untreated control group. During treatment, 19 of 40 animals showed heat and ovulated; CAP was discontinued and all animals bred. Sixteen out of 19 animals conceived. Within 21 days after CAP withdrawal, 12 mares came in heat and 11 conceived. Of 40 treated animals, 37 (92.5%) came into estrus, and 31 became pregnant (77.5%); while 8 of 15 control mares started cycling during the season (53.3%) and only 5 (33.3%) conceived. This treatment effect is significant (p

Summary The mechanisms involved in the interaction of complement components with sensitized equine arteritis virus (EAV) were investigated. Virus neutralization and virolysis depended on both the concentration of the complement components and the concentration of the sensitizing antibody. High concentrations of C4, 2 and 3, with an optimal concentration of C1, were sufficient for neutralizing virus infectivity in the presence of excess antibody. The addition of the remaining five components (C5 to C9) of the complement system induced lysis of the previously neutralized virus particle. Lysis was initiated by C8 and was augmented by C9. Components C5 to C9 did not enhance neutralization produced by excess antibody and limiting concentrations of complement components. In contrast, addition of components C5 to C9 enhanced neutralization by means of lysis of the virus particle under conditions of low antibody concentration.

Equine abortion virus (EAV), a herpesvirus, agglutinates horse red blood cells (RBC). The hemagglutinin appears to be an integral part of the viral envelope and is not “soluble” as was formerly anticipated. The hemagglutination proved to be stable at 4 °, 20 °, and 37 °, and could not be reversed by Vibrio cholerae neuraminidase. Trypsin could not be used for reversion since RBC treated with trypsin proved to be nonagglutinable by EAV. The hemagglutinating (HA) activity was destroyed by dithiothreitol indicating the role of disulfide groups in hemagglutinin. The HA activity was also destroyed by proteolytic enzymes (trypsin, α-chymotrypsin, or Pronase), but proved to be resistant to the action of lipid solvents (chloroform or ether) or phospholipase C. The EAV hemagglutinin is thus a protein, the activity of which is not dependent on lipids. In fresh virus harvests the HA titers were directly proportional to infectivity titers, 1 HA unit being equal to about 10 7.0 plaque-forming units in PK-15 cells. In virus preparations, purified from such harvests, 1 HA unit was found to be equal to approximately 0.65 μg protein. These figures might explain why the antibody response to hemagglutinin was poor following immunization by natural infection or vaccination.

Mice, guinea pigs, and duck embryo cell cultures were inoculated with known subtypes of Venezuelan equine encephalomyelitis (VEE) virus and the attenuated (TC-83) strain of VEE. With the exception of TC-83, all strains were highly pathogenic for suckling mice by either intracranial or intraperitoneal routes of inoculation used. Virulence for older mice and guinea pigs provided a means to distinguish strains. In addition, virulence or lack of virulence for adult mice or guinea pigs provides a rapid method for separating epizootic subtype IB from TC-83 VEE virus isolates.

Long-term suspension cultures were established from the thoracic duct lymph and pericardial effusion of a horse with histopathologically confirmed lymphosarcoma. Chromosome studies have shown that all cultures are aneuploid, suggesting that the cultured cells are neoplastic and are derived from the neoplastic cells of the diseased animal. Preliminary electron microscope studies on the untreated long-term cultures and on phytohemagglutinin-treated cells have failed to reveal virus-like particles.