Acid-induced autoagglutination found in chicken pathogenic Escherichia coli strain.

Chicken pathogenic Escherichia coli strains were found to autoagglutinate in a static culture of trypticase soy broth (TSB). One strain, designated PDI-386, was further studied for its autoagglutinating property. Acidity in the cultured medium caused by glucose degradation induced the autoagglutination. The bacterial cells grown in a glucose-free L-broth could be aggregated by adding acid, which suggests a potentiality of autoagglutination of the strain grown in the L-broth. The autoagglutinating parent (Agg) formed small colonies with irregular edges like rough colonies on the TS agar, whereas its non-autoagglutinating variant (Nag) formed larger smooth colonies with a perfectly round edge. The Nag colony was easily generated from the Agg colony on the TS agar. The autoagglutinating property was very unstable when the bacteria was passed in the TSB, but rather stable in the L-broth. Under electron microscope, the Agg were found to possess pili of more than 20 microns in length. However, the phenotypic expression of autoagglutination did not correlate with that of mannose-sensitive hemagglutination against guinea pig erythrocytes. Incubation of the Nag in the L-broth at room temperature for more than 10 days provoked the reversion of the autoagglutination. There was no difference between the Agg and the Nag in terms of surface hydrophobicity, sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) patterns of membrane proteins and LPS, and plasmid profiles. The virulence of the Agg was higher than that of the Nag. The autoagglutination property is, however, so unstable that the pathogenicity of E. coli isolates from chickens should be carefully evaluated.     

Skeletal muscle fiber size in untrained and endurance-trained horses.

The mean area and minimal diameter of 3 histochemically determined myofiber types (1, 2A, and 2B; myosin ATPase in acid buffer) were calculated in middle gluteal muscle biopsy specimens from 62 stallions, 47 Andalusians and 15 Arabians, ranging in age from 6 to 12 years. Fourteen Andalusians and 7 Arabians were untrained, and the remainder were actively endurance-trained. The 6-month training schedules involved walking, slow trotting, and cantering. Fourteen Andalusians were moderately endurance-trained, whereas the other 19 Andalusians and 8 Arabians were strongly endurance-trained. Significant differences were not recorded between untrained and endurance-trained Arabians with respect to the area (type 1, 3,194 +/- 869 microns 2 and 3,150 +/- 370 microns 2; type 2A, 3,819 +/- 890 microns 2 and 3,380 +/- 356 microns 2; and type 2B, 4,872 +/- 962 microns 2 and 4,417 +/- 646 microns 2) or minimal diameter (type 1, 52.2 +/- 7.4 microns and 52.8 +/- 3.1 microns; type 2A, 58.1 +/- 6.7 microns and 55.0 +/- 2.8 microns; and type 2B, 65.3 +/- 6.4 microns and 63.4 +/- 4.3 microns) of the 3 fiber types, nor between untrained and endurance-trained Andalusians with respect to the area (untrained, 3,990 +/- 690 microns 2; moderately endurance-trained, 3,882 +/- 347 microns 2; and strongly endurance-trained, 3,758 +/- 510 microns 2) and minimal diameter (untrained, 58.1 +/- 4.7 microns; moderately endurance-trained, 59.7 +/- 2.7 microns; and strongly endurance-trained, 58.7 +/- 4.5 microns) of 2A fibers.(ABSTRACT TRUNCATED AT 250 WORDS)     

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.     

Infection of bovine fetuses at 120 days' gestation with virulent and avirulent strains of bluetongue virus serotype 11.

Bluetongue virus infection in sheep and cattle during fetal development causes neuropathology. Two strains of bluetongue virus serotype 11 designated as UC-2 and UC-8 have different virulence patterns in newborn mice. These viruses have distinctly different electropherotype patterns on polyacrylamide gel electrophoresis indicating a genetic difference in these two viruses of the same serotype. Four bovine fetuses each were inoculated intramuscularly with either UC-2 or UC-8, and one fetus was inoculated with placebo. The inoculation was made intramuscularly through the uterine wall at 120 days' gestation, and the bovine fetuses were recovered by cesarean section 12 or 20 days after inoculation. Fetal blood was collected for virus isolation and serology. Virus was reisolated from brain, blood, lung and liver. Both strains, UC-2 and UC-8, cause severe lesions in the 120 day fetuses. The encephalomalacic lesions occurred earlier and were more severe in fetuses inoculated with UC-8 as compared to those inoculated with UC-2. The subtle differences observed in the fetuses inoculated with the two different strains suggest that there is a difference in pathogenic potential of the two viruses. These differences do not appear to be completely dependent upon the host species.     

Feline immunodeficiency virus neurotropism: evidence that astrocytes and microglia are the primary target cells.

To investigate the neuropathogenesis of feline immunodeficiency virus (FIV) infection in vitro, we have utilized three populations of cultured feline neural cells (astrocytes, microglia, brain endothelium) to assess the relative susceptibility to FIV infection, ability to produce viral antigens, and effects of infection on cell survival. Astrocytes appeared to be the most susceptible to infection, followed by microglia, whereas brain endothelial cells were relatively resistant to infection. Astrocyte infection resulted in syncytium formation and cell death, while microglial cells remained persistently and productively infected, without obvious cytopathic effects. These results suggest that FIV entry into the central nervous system probably does not occur via infected endothelium and that both astrocytes and microglia are more likely target cells for the virus.     

In vitro nitroimidazole resistance of Trichomonas gallinae and successful therapy with an increased dosage of ronidazole in racing pigeons (Columba livia domestica)

Six out of eight different Trichomonas gallinae strains isolated from racing pigeons proved to be resistant to the nitroimidazole drugs ronidazole, carnidazole and metronidazole. The minimal cytocidal concentration of ronidazole was determined in in vitro experiments. Moreover, a therapeutic dose for ronidazole was determined for the control of trichomoniasis in pigeons from which the resistant T. gallinae strains were isolated. It was a 5-fold increase of the recommended ronidazole dosage which eliminated the infection in affected pigeons.     

Characterization of phosphate species in urban sewage sludges by high-resolution solid-state 31P NMR

The mineral forms of phosphorus in three urban sewage sludges were characterized using high-resolution solid-state phosphorus-31 nuclear magnetic resonance (NMR) coupled to a sequential extraction. The sludges studied were an anaerobically-digested and heat-treated sludge (Paris-Achères), an activated sludge (Briare) and an anaerobically-digested sludge (Nancy). NMR observations were conducted using both single-pulse and cross-polarization sequences in order to distinguish between ³¹P nuclei far from ¹H nuclei, and ³¹P located within a fraction of a nanometre of ¹H. This approach showed that a complex mixture of P species was present in these sludges. A mixture of hydrogenated octocalcium phosphates and apatites was observed in the three samples. Monetite was present in the anaerobically-digested sludge and brushite in the activated sludge. Dehydrogenated condensed calcium phosphates (compounds with a Ca:P ratio higher than 1.0 such as fluorapatite or tricalcium phosphate) and dehydrogenated pyrophosphates were also probably present in the anaerobically-digested sludge. A poorly-ordered wavellite was observed in the three sludges after the HCl extraction. However, results were inconclusive as to whether this mineral was present in the three sludges, or had been precipitated during the sequential extraction.     

Xylazine and tiletamine-zolazepam anesthesia in horses

The cardiopulmonary and anesthetic effects of xylazine in combination with a 1:1 mixture of tiletamine and zolazepam were determined in 6 horses. Each horse was given xylazine IV or IM, as well as tiletamine-zolazepam IV on 4 randomized occasions. Anesthetics were administered at the rate of 1.1 mg of xylazine/kg of body weight, IV, 1.1 mg of tiletamine-zolazepam/kg, IV (treatment 1); 1.1 mg of xylazine/kg, IV, 1.65 mg of tiletamine-zolazepam/kg, IV (treatment 2); 1.1 mg of xylazine/kg, IV, 2.2 mg of tiletamine-zolazepam/kg, IV (treatment 3); and 2.2 mg of xylazine/kg, IM, 1.65 mg of tiletamine-zolazepam/kg, IV (treatment 4). Tiletamine-zolazepam doses were the sum of tiletamine plus zolazepam. Xylazine, when given IV, was given 5 minutes before tiletamine-zolazepam. Xylazine, when given IM, was given 10 minutes before tiletamine-zolazepam. Tiletamine-zolazepam induced recumbency in all horses. Duration of recumbency in group 1 was 31.9 +/- 7.2 (mean +/- 1 SD) minutes. Increasing the dosage of tiletamine-zolazepam (treatments 2 and 3) significantly (P less than 0.05) increased the duration of recumbency. Xylazine caused significant (P less than 0.05) decreases in heart rate and cardiac output and significant (P less than 0.05) increases in central venous pressure and mean pulmonary artery pressure 5 minutes after administration. Respiratory rate was decreased. Arterial blood pressures increased significantly (P less than 0.05) after xylazine was administered IV in treatments 1 and 3, but the increases were not significant in treatment 2. Xylazine administered IM caused significant (P less than 0.05) increases in central venous pressure and significant (P less than 0.05) decreases in cardiac output.(ABSTRACT TRUNCATED AT 250 WORDS)