Preliminary observations on the experimental transmission of scrapie to elk (Cervus elaphus nelsoni) by intracerebral inoculation.

To determine the transmissibility of scrapie to Rocky Mountain elk (Cervus elaphus nelsoni), six elk calves were inoculated intracerebrally with brain suspension from sheep naturally affected with scrapie. One elk developed a brain abscess and was euthanatized at 7 weeks postinoculation (PI), and two others died at 6 and 15 months PI because of physical injuries. At 25 and 35 months PI, two other elk died after brief terminal neurologic episodes. Necropsy of these revealed moderate weight loss but no other gross lesions. Microscopically, characteristic lesions of spongiform encephalopathy were seen throughout the brains and the spinal cords, and in both cases these tissues were positive for PrP(res) by immunohistochemistry. Brains of both animals were positive for PrP(res) by western blot and for scrapie-associated fibrils (SAFs) by negative stain electron microscopy. PrP(res) and SAFs were not detected in the three elk that died or were euthanatized because of coincidental causes. Over 3.5 years after initiation of this experiment, the one remaining inoculated elk and two uninoculated (control) elk are alive and apparently healthy. These preliminary findings demonstrate that 1) sheep scrapie agent can be transmitted to elk by intracerebral inoculation; 2) the infection can result in severe, widely distributed spongiform change and accumulations of PrP(res) in the central nervous system (CNS); and 3) based on the examination of a limited number of CNS sections from two cases, this condition cannot be distinguished from chronic wasting disease with currently available diagnostic techniques.

Pathogenesis of infection induced by an adenovirus isolated from a goat.

OBJECTIVE: To determine the pathogenic potential of an adenovirus isolated from a goat. ANIMALS: 14 colostrum-deprived, isolation-reared goat kids approximately 3 weeks old. PROCEDURE: Kids were inoculated with either cell culture fluid containing adenovirus (n = 10) or uninfected cell culture fluid (n = 4): 2 ml transtracheally and 1 ml/nostril. Clinical signs of disease and rectal temperature were recorded daily; nasal secretion and fecal specimens were collected daily. Control kids were necropsied, 2/d, on postinoculation days (PID) 5 and 10. Virus-inoculated kids were necropsied on PID 3, 5, 7, 10, and 28. After necropsy, lung, liver, kidney, and brain specimens were aseptically collected for virus isolation attempts. Tracheal fluid was collected on sterile cotton swabs. Turbinate, trachea, lung, mediastinal lymph node, liver, kidney, duodenum, jejunum, ileum, mesenteric lymph node, colon, and brain specimens were collected for histologic evaluation. RESULTS: Kids developed mild-to-moderate clinical respiratory tract infection. Virus was recovered consistently from nasal secretion and sporadically from fecal specimens. Grossly, there were multiple areas of atelectasis and hyperemia, principally in the cranioventral portion of the lungs. Microscopically, there was detachment and sloughing of foci of epithelial cells of the terminal bronchioles and alveoli. In kids necropsied late in the disease, these changes were accompanied by hyperplasia of type-II epithelial cells. Viral inclusions were not an obvious feature, but a few cells contained probable inclusions. CONCLUSIONS AND CLINICAL RELEVANCE: The caprine adenovirus reported here is capable of inducing respiratory tract disease and lesions in the lungs of young kids.

Evaluation of ethylenediaminetetraacetic acid, tetrasodium salt dihydrate (EDTA)-Tween 20 treatment versus protease digestion of formalin-fixed tissue sections for detection of bovine respiratory syncytial virus antigen in infected ovine lung.

The efficacy of protease and ethylenediaminetetraacetic acid, tetrasodium salt dihydrate (EDTA)-Tween 20 in unmasking bovine respiratory syncytial virus (BRSV) antigens in formalin-fixed lung tissue was compared using avidin-biotin immunoperoxidase procedure. Tissues were taken from experimentally infected lambs. BRSV antigen stained in both techniques. Treatment with EDTA-Tween 20 resulted in more intense staining of BRSV infected cells, more uniform cytoplasmic staining, less non-specific background, and superior cellular detail in comparison to protease digestion.

Susceptibility of colostrum-deprived swine of various ages to streptococcic lymphadenitis.

The effect of age on susceptibility of young pigs to streptococcic lymphadenitis was investigated. Twenty-nine cesarean-derived, colostrum-deprived pigs were allotted to 7 groups exposed to type IV group E Streptococcus (GES) at 5, 14, 28, 35, 56, 70, and 84 days of age. Four cesarean-derived, colostrum-deprived pigs were maintained as nonexposed controls. Six naturally farrowed, susceptible controls were exposed to GES at 63 to 84 days of age. All exposed pigs were killed and necropsied 28 days after exposure. Lesions of streptococcic lymphadenitis were not observed in pigs exposed at 5 or 14 days of age, except for 1 microabscess in a mandibular lymph node in a pig exposed at 14 days, but GES was recovered from 11% of lymph nodes examined from pigs of those age groups. Lesions and GES-positive lymph nodes were frequent in cesarean-derived, colostrum-deprived pigs exposed at 28 days and older and in susceptible controls. Serologic response to exposure, as determined by microtitration agglutination test and bactericidal test, was observed only in pigs exposed at 14 days and older. The absence of abscess development in pigs exposed at 5 or 14 days of age was not caused by antibody or failure of infecting organisms to reach the target organs.

Intrauterine transmission of ovine progressive pneumonia virus.

Ovine fetuses, newborn lambs, and ovine colostrum were examined for ovine progressive pneumonia virus. The lambs and colostrum were also examined for specific antibody. Virus was isolated from 1 fetus, from 2 newborn lambs, and from most samples of colostrum. The fetus was about 100 days old and was carried by a seronegative ewe in contact with seropositive sheep. Both newborn lambs were carried by seropositive ewes. One lamb was dead at birth; the other lamb was normal and had not nursed. Antibody specific for the virus was present in the colostrum of 12 of 14 seropositive ewes and in the serum of 8 of 11 lambs that had nursed seropositive ewes, but not in the serum of lambs that had not nursed.

Lesions and pathogenesis of disease in young calves experimentally induced by a bovine adenovirus type 5 isolated from a calf with weak calf syndrome.

Lesions induced in each of 9 young colostrum-deprived calves closely resembled lesions seen in naturally occurring "weak calf syndrome" of eastern Idaho and southwestern Montana. The disease was experimentally induced by intravenous injection of bovine adenovirus type 5 that had been isolated from a calf with weak calf syndrome...

Fetal mummification associated with porcine parvovirus infection.

A crossbred gilt farrowed 2 mummified fetuses at term, but subsequently developed uterine inertia and became listless. The remaining 5 fetuses of the litter (4 mummified and 1 normal appearing) were collected by hysterectomy. Porcine parvovirus (PPV) was isolated from tissues of the mummified fetuses, and masses of viral antigen were detected throughout the same tissues when cryostat sections were examined by immunofluorescence microscopy. Serum from the normal-appearing fetus of this litter had a hemagglutination inhibition (HI) titer for PPV of 320. The finding of antibody (HI titer of 1,280) in serum collected from the gilt on the day of farrowing, but not in serum collected 67 days before, indicated initial exposure to PPV during gestation.