Studies on the pathogenesis of epizootic bovine abortion.

Ornithodoros coriaceus Koch ticks were fed on 37 pregnant cows. The fetuses were obtained from the cows at 23 to 126 days after maternal tick exposure. Characteristic lesions of epizootic bovine abortion were observed only in those fetuses recovered 100 days more or after maternal tick exposure. Fetuses collected between 50 and 100 days showed mild-to-moderate lymphoid and mononuclear cell hyperplasia. Reaction in fetuses studied less than 50 days after maternal tick exposure were mild. Lesions could not be seen in 2 of the youngest fetuses. Increases in serum immunoglobulin concentrations were present only in those fetuses examined 80 days or more after their dams had been exposed to ticks. The specificity of the immunoglobulins could not be determined. Sera from 12 fetuses tested failed to fix complement in tests for group-specific chlamydial antibodies. A wide variety of microbiological cultivation attempts were made to recover the causative agent of epizootic bovine abortion from these fetuses; however, no agent was recovered regularly, and chlamydial organisms were not recovered from any. The significance of 2 recovered agents, apparently viral, is still to be determined. Fetal tissues, both frozen and fresh, collected from fetuses of dams exposed to a feeding of ticks were capable of reproducing the disease after inoculation into pregnant cows or directly into fetuses.

Effect of intrauterine saline infusion during the late luteal phase on the estrous cycle and luteal function of the mare.

The intrauterine infusion of 500 ml of warm sterile saline solution into mares on days 12, 13, or 14 after ovulation failed to alter the ovulatory interval, although intervals were shorter for days 12 and 13 (20.6 days) when compared with those in control mares (21.6 days). The IU fusion shortened luteal-life-span on days 12 (12.0 vs 13.8 days) and 13 (13.0 vs 14.4 days) (P is less than 0.05), but not day 14 (14.0 vs 13.5 days), when comparing the effects of IU infusion with an average of before and after base-line data. There was no effect on the interval from corpus luteum regression to ovulation, ie, the final follicular phases. The treatment average for days 12 and 13 combined was 7.7 days vs 7.3 days for controls. Also, no significant effect was observed for the duration of estrus in that the treatment average for days 12 and 13 was 5.1 days, and for controls, 6.0 days. The infusion of saline solution caused an immediate release of prostaglandin F(2alpha) within 5 minutes, with additional large releases occurring over the next 24 hours. Progestin concentrations decreased rapidly in relation to this prostaglandin release.

Immunity to equine herpesvirus 1 infection in foals during the first year of life.

A band of 23 pregnant mares on a Thoroughbred breeding farm all had serum virus-neutralizing antibody titres to equine herpesvirus 1 (EHV-1). Antibody was not transferred to their foals in utero. All foals received antibody from colostrum and developed antibody titres similar to their dams. The serum virus-neutralizing antibody titres were observed in 10 of these foals for 1 year. Decay of passive immunity occurred at the rate of 3.25 two-fold dilutions in 100 days and reached zero at the mean time of 180 days. The foals were exposed to EHV-1 twice. Foals with a geometric mean titre of 1 : 25 experienced infection and a rise of titre, while those with a geometric mean titre of 1 : 76 resisted infection.

Hoof overgrowth in Holstein--Friesian dairy cattle.

The genetic etiology of hoof overgrowth, a widespread problem in Holstein-Friesian cattle, was examined. Although all four feet are affected, the hind feet usually have a greater degree of overgrowth. There is a distinct age tendency for the trait; the younger cows' hooves grow faster than those of the older cows, but the overgrowth in older cows reaches greater proportions. Analysis of variance of chi-square frequency tests showed that there is a component of heritability involved in the expression of the trait, but that it follows a more complex model than a simple autosomal recessive gene would show.

Equine herpesvirus 1 infection of horses: studies on the experimentally induced neurologic disease.

Experimental infection with equine herpesvirus 1 (rhinopneumonitis) resulted in neurologic disease in 8 of 15 inoculated horses. Nonpregnant animals did not develop clinical disease, and microscopic examination of tissues revealed no changes. In all mares between 3 and 9 months of gestation, a neurologic syndrome appeared 6 to 8 days after inoculation. Mares inoculated when 10 months pregnant did not develop neurologic disorders, but several aborted. The histopathologic change common to both sequelae was vasculitis, involving smaller arteries and veins. Although blood vessel changes were detected in endometrium of all pregnant mares, vascular changes were present in the central nervous system only in mares having neurologic disease. Concomitant degeneration of nervous tissue occurred within the central nervous system and, in many sites, anatomic and temporal relationships of vasculitis and nervous tissue degeneration suggested a cause-effect relationship. This theory was strengthened by the lack of usual histopathologic indications of encephalomyelitis. In cerebrospinal fluid from affected mares, there was an increase in protein but not pleocytosis.