Observations on transplacental infection with bluetongue virus in sheep

Twenty-four ewes were inoculated with 1 of 2 strains of bluetongue virus type 4 at 40, 60, or 80 days of gestation. Two ewes aborted, 2 ewes died, and 1 was killed during the experiment, but their fetuses were recovered. At term, 2 mummified fetuses, 4 dead lambs, and 17 clinically healthy lambs were produced by 12 sheep, and the remaining 7 sheep were barren. Porencephaly and cerebellar dysgenesis were found in term lambs born to sheep inoculated at 40 and 60 days of gestation. Radiographic examination of 12 fetuses showed developmental ages far less than their chronologic age; 8 fetuses had skeletal growth-retardation lines, which were also observed in the dead lambs. A systemic lymphoreticular hyperplasia was observed in the dead lambs and in all lambs at 12 weeks of age; in 4 of the latter, granulomatous reactions were present in the liver and kidney. Lungs of the full-term lambs were reduced in weight and showed poor alveolar development and mononuclear cell infiltration, which persisted in the 12-week-old lambs. It was concluded that bluetongue virus is capable of causing not only gross abnormalities of the CNS, but also generalized growth retardation and fetal lymphoreticular hyperplasia.     

Crystalluria. Observations, interpretations, and misinterpretations

Crystalluria results from oversaturation of urine with crystallogenic substance. However, oversaturation may occur as a result of in vitro as well as in vivo events. The microscopic appearance of crystals only represents a tentative identification of their composition because variable conditions associated with their formation, growth, and dissolution may alter their appearance. Definitive identification is dependent on physical methods such as optical crystallography, x-ray diffraction, and electron microscopic analysis.     

Association of tumor-associated antigen on the proliferation of bovine leukemia virus-infected lymphoblastoid B-cell lines.

The association of tumor-associated antigen (TAA) on the proliferation of BLV-infected lymphoblastoid B-cell lines (BL2M3 and BL312) was investigated. Flow cytometric analysis of the expression of TAA with monoclonal antibody (mAb) c143 showed high expression of TAA on the surfaces of BL2M3 and BL312 cells. A large amount of TAA was found in the culture supernatant of BL2M3 and BL312 cells as well as in the lysates of BL2M3 and BL312 cells. Culture supernatant but not lysates of BL2M3 and BL312 cells promoted the growth of either BL2M3 cells or BL312 cells. Furthermore, this growth promoting activity in culture supernatants of BL2M3 and BL312 cells was inhibited in a dose-dependent manner when cultured with mAb c143. These results suggested that TAA may be involved in the growth factor-mediated cell growth of bovine B-lymphoblastoid cell lines expressing TAA on their cell surface.     

Inherited hyperchylomicro-naemia in the cat: Lipoprotein lipase function and gene structure

Hyperchylomicronaemia was identified in a four-week-old Siamese kitten with lethargy, in-appetence, hindlimb ataxia and profound anaemia. The kitten was euthanased and at necropsy a thrombus was found occluding the caudal aorta. Two littermates later presented with lethargy, inappetence and hypertriglyceri-daemia which resolved after being weaned on to a low fat diet. A similar condition was subsequently diagnosed in a kitten born to the same sire but a different queen. The expression of hyperchylomicronaemia in two related litters was suggestive of an inherited, familial defect in the function of lipoprotein lipase (LPL). The activity of this enzyme was reduced in all three parents, the two recovered cases and two related, but apparently unaffected kittens, compared with a control group of unrelated cats belonging to the breeder. This reduction in activity was not attributable to defective activation of LPL by its serum cofactor apolipoprotein C-II or the presence in plasma of a factor that inhibited LPL. The gene that codes for LPL was examined by restriction fragment length polymorphism analysis using a human LPL cDNA probe. The results showed that the cat has a similar, but not identical, LPL gene to man. However, there were no differences in the restriction fragment patterns obtained from affected, unaffected and control animals.     

Differential leucocyte responses to various degrees of food restriction in broilers, turkeys and ducks.

1. White blood cell responses of broilers, turkeys and ducks were examined at regular intervals after being subjected to various degrees of food restriction. 2. Restricted-fed broilers showed increases in heterophil and basophil numbers, together with a corresponding decrease in lymphocytes. The heterophil/lymphocyte ratio was raised. There were no differences between broiler strains. 3. After only one week of feeding restricted diets, heterophils were significantly raised in selected and unselected 2-week-old ducks. At 21 weeks of age, those ducks receiving 50% of food required to achieve their ad libitum-fed body weight had raised heterophils. 4. Ducks receiving food to achieve 25% of ad libitum-fed birds produced a marked basophilia, but no heterophilia. 5. After two weeks of food restriction, turkeys responded with significant heterophil/lymphocyte ratios following two degrees of restricted feeding. 6. It was concluded that in some poultry, a heterophilia may be the response to mild to moderate stress but a basophilia may result after severely stressing birds.     

Pathogenicity of porcine enterotoxigenic Escherichia coli that do not express K88, K99, F41, or 987P adhesins.

Three-week-old weaned and colostrum-deprived neonatal (less than 1 day old) pigs were inoculated to determine the pathogenicity of 2 enterotoxigenic Escherichia coli isolates that do not express K88, K99, F41, or 987P adhesins (strains 2134 and 2171). Strains 2134 and 2171 were isolated from pigs that had diarrhea after weaning attributable to enterotoxigenic E coli infection. We found that both strains of E coli adhered in the ileum and caused diarrhea in pigs of both age groups. In control experiments, adherent bacteria were not seen in the ileum of pigs less than 1 day old or 3 weeks old that were noninoculated or inoculated with a nonpathogenic strain of E coli. These control pigs did not develop diarrhea. Antisera raised against strains 2134 and 2171 and absorbed with the autologous strain, grown at 18 C, were used for bacterial-agglutination and colony-immunoblot assays. Both absorbed antisera reacted with strains 2134 and 2171, but not with strains that express K99, F41, or 987P adhesins. A cross-reaction was observed with 2 wild-type K88 strains, but not with a K12 strain that expresses K88 pili. Indirect immunofluorescence with these absorbed antisera revealed adherent bacteria in frozen sections of ileum from pigs infected with either strain. We concluded that these strains are pathogenic and express a common surface antigen that may be a novel adhesin in E coli strains that cause diarrhea in weaned pigs.     

Biopsy of the bovine mammary gland.

A technique is described for biopsy of the bovine udder, employing sedation and local anaesthesia. Tissue samples of approximately 5 g were obtained by electrocautery from two quarters of the udder of a cow laterally recumbent. Care was taken to ensure complete haemostasis which was achieved by electrocoagulation and ligation. Postoperative recovery was rapid, and loss of yield was no greater in biopsied glands than in control glands of the same cow. Yield from all quarters returned to preoperative levels within 48 h.     

5-bromo-2'-deoxyuridine blocks myogenesis by extinguishing expression of MyoD1

The pyrimidine analog 5-bromodeoxyuridine (BUdR) competes with thymidine for incorporation into DNA. Substitution of BUdR for thymidine does not significantly affect cell viability but does block cell differentiation in many different lineages. BUdR substitution in a mouse myoblast line blocked myogenic differentiation and extinguished the expression of the myogenic determination gene MyoD1. Forced expression of MyoD1 from a transfected expression vector in a BUdR-substituted myoblast overcame the block to differentiation imposed by BUdR. Activation of BUdR-substituted muscle structural genes and apparently normal differentiation were observed in transfected myoblasts. This shows that BUdR blocks myogenesis at the level of a myogenic regulatory gene, possibly MyoD1, not by directly inhibiting the activation of muscle structural genes. It is consistent with the idea that BUdR selectively blocks a class of regulatory genes, each member of which is important for the development of a different cell lineage.