Three Beagles with chronic anemia and reticulocytosis were studied. The dogs originated from a large breeding colony and appeared clinically normal with the exception of splenomegaly. The PCV ranged from 30 to 39% (normal, 46 to 56%), with reticulocyte indices of 2.3 to 9.9. Red blood cells were morphologically normal, and examination of marrow aspirates revealed erythroid hyperplasia. Shortened chromium-51 RBC life-spans (7.2 to 15.4 days in anemic dogs; 22.2 to 25.2 days in control dogs) documented a hemolytic anemia. Acquired causes of hemolytic anemia were ruled out. Red blood cells had normal glycolytic enzyme activities, no evidence of unstable or abnormal hemoglobin, and had altered osmotic fragility curves. The breeding of 2 anemic dogs resulted in off-spring with anemia and reticulocytosis. Polyacrylamide gel electrophoresis revealed no abnormalities in RBC membrane cytoskeletal proteins in all anemic adult dogs and in 3 offspring.

Morphologic lesions seen in six 8-month-old Labrador Retrievers with hereditary myopathy were predominantly small- and large-group atrophy of muscle cells of all fiber types. The dogs were intolerant of excerise and fatigued rapidly. An isolated gracilis muscle preparation was used to study the hemodynamic features of the microvasculature. Isogravimetric capillary pressure as well as arterial and venous pressures in the isolated gracilis muscle preparation obtained during maximal vasodilatation were within the range reported for healthy, mixed-breed dogs, as were precapillary, postcapillary, and total vascular resistances. Capillary filtration and osmotic reflection coefficients were not different from those reported in other studies on healthy dogs. All measurements and calculations were reported during reperfusion, subsequent to a 4-hour period of global ischemia. Postischemic vascular responses were similar to the pattern previously reported in healthy dogs. These studies did not support the hypothesis of a vascular defect as a cause of hereditary myopathy in Labrador Retrievers.

Lymphocytes from 5 clinically normal lambs and 5 lambs affected with ovine hereditary chondrodysplasia (spider syndrome) were cultured, G-banded, and karyotyped. Fifty metaphase karyotypes and one heterogram were evaluated for chromosome number and morphologic features. All lambs had normal diploid (2n) chromosome numbers of 54,XX or 54,XY, and there were no apparent differences in the morphologic features of the chromosomes.

Experiments concerned with the immunogenicity, pathogenicity, and transmissibility of a recombinant vaccinia:Sindbis virus were conducted. The WR strain of the recombinant vaccinia:Sindbis virus was found to be infective for calves and mildly pathogenic, resulting in local tissue reaction. It was not transmissible to other calves. Also, it was found to be immunogenic when inoculated intradermally into calves, and antibody was produced against the parent vector virus (vaccinia) and the Sindbis antigen. Recombinant virus given IV to calves induced no detectable clinical signs, nor did the calves develop neutralizing antibodies. Furthermore, second-passage lesion material containing up to 10(7) tissue culture infective doses of the recombinant virus failed to induce development of lesions or illness in intradermally inoculated calves, and virus could not be recovered from the inoculation sites. In this series of experiments, this vaccinia recombinant given intradermally was immunogenic, mildly pathogenic at the local injection site only, and was not transmissible to contact animals, thus demonstrating the potential efficacy and safety of the WR strain of vaccinia virus when used as a live vector system in cattle.

Holstein cow 1 was examined because of skin fragility and delayed healing of skin wounds, which were markedly exacerbated around the time of parturition. A skin biopsy sample was obtained, and light microscopy revealed irregular deposition of thin collagen fibers in a dermal matrix. Although diffuse inflammation did not occur, the number of plump fibroblasts was increased. Electron microscopy revealed poor construction of collagen fibrils in the dermal matrix. Biochemical analysis of the dermis revealed a normal amount of collagen and uronic acid, but sodium dodecyl sulfate-polyacrylamide gel electrophoresis reveled an increased proportion of soluble alpha-, beta-, and gamma-collagen chains of normal molecular weights. Neither procollagen nor its intermediates devoid of amino- or carboxy-terminal extension peptide were observed. Dermal collagen from cow 1 was more soluble in a neutral salt solvent, 0.5M acetic acid, and the acid containing pepsin than was dermal collagen from healthy cow 2. The peptic digestion profile of dermis from cow 1 revealed a lowered degree of intermolecular cross-linking and destabilization of helical structure in the dermis collagen. The extrahelical peptic cleavage of collagen before cyanogen bromide digestion resulted in release of more fragments derived from carboxy-terminal part of alpha1 chains in dermis of cow 1 than in dermis of healthy cow 2.

A bovine herpesvirus-1 (BHV-1) isolate (FI) from an aborted fetus was used to infect 9 heifers at various stages of gestation. Two heifers were inoculated IV on postbreeding day (PBD) 1, 7, or 14, and 3 heifers were inoculated in the sixth month of pregnancy. Plasma progesterone assays were used to monitor corpus luteum function in heifers inoculated during early pregnancy. Low progesterone values and infertility were seen in the 2 heifers inoculated on PBD 1. Luteal function remained normal in heifers inoculated on PBD 7 or 14. These 4 heifers inoculated on PBD 7 or 14 carried their fetuses to term, and their calves were free of BHV-1 infection at birth. Three heifers inoculated during the sixth month of pregnancy also carried their fetuses to term. Two calves were born alive, and BHV-1 was not isolated from nasal swab samples of either calf; the third calf was stillborn. Virus was not isolated from the stillborn calf's tissues, but BHV-1 was isolated from the placenta. Lesions were not detected in several tissues examined by light microscopy, and BHV-1 antigen was not detected by immunohistochemical examination of paraffin sections. Restriction endonuclease analysis of viral DNA was used to compare the FI virus to other BHV-1 isolates (Colorado-1, Iowa, and K22). On the basis of restriction endonuclease analysis, the FI isolate should be classified as a type-2 (infectious pustular vulvovaginitis) virus, specifically subtype a.

A genomic probe specific for malignant catarrhal fever (MCF) virus was cloned by using purified viral DNA from MCF-virus strain WCll. Restriction endonuclease analysis of the purified viral DNA was used to identify the cloned viral genomic fragment. Dot blot hybridization by use of the genomic probe (pRP-5) indicated that the probe hybridized specifically with WCll-MCF virus, as well as with one other isolate of MCF-associated herpesvirus. Hybridization also was observed to a non-MCF virus strain of bovine herpesvirus.