Correlation of serum antibody titer for avian encephalomyelitis virus (AEV) in hens with the resistance of progeny embryos to AEV

Serum antibody titers for avian encephalomyelitis virus of vaccinated breeding hens were correlated with the resistance of the hens' progeny embryos to viral challenge. All of the embryos from hens that had enzyme-linked immunosorbent assay titers greater than 400 were resistant to challenge, and two-thirds of the embryos from hens that had titers greater than 300 were resistant. About one-half of the embryos from hens that had titers from 100 to 300 were immune to challenge.     

Experimental infection of normal and immunosuppressed pigs with Pseudomonas pseudomallei

A single dose of 5 x 10(8) bacilli of Pseudomonas pseudomallei by intratracheal injection resulted in acute (21 cases) or chronic (19 cases) melioidosis in 40 of 48 pigs. Fifteen (10 acute and 5 chronic) had been immunosuppressed by cyclophosphamide before inoculation. The major clinical signs were initial fever, marked neutrophilia and, in the acute cases, respiratory distress. There were no signs of the nasal and ocular discharge, paresis or diarrhoea seen in acute cases in south-east Asia. The cyclophosphamide treatment caused a significant decrease in the neutrophil count by 7 d after inoculation in all 15 immunosuppressed pigs, and all were culture positive at necropsy. Eight of the 33 non-treated pigs were culture negative at necropsy. Pigs overcoming the initial phase of infection had more abscess-like nodules that were bacteriologically sterile at necropsy than the pigs with acute cases of melioidosis. P. pseudomallei was isolated predominantly from the spleen, lungs and the injection site. Although only one strain was used in this study, it is likely that Australian strains of P. pseudomallei are not as virulent as the south-east Asian isolates.     

Monoclonal antibodies that distinguish bovine T and B lymphocytes

The specificities of three monoclonal antibodies (MAbs) were investigated using microcytotoxicity, fluorescence microscopy and laser flow cytometry (LFC) techniques. By microcytotoxicity, bovine thymocytes (n = 4) were estimated to be 85% B26A+, 4% TH21A+, and 1% H4+. Nylon wool enriched peripheral blood T lymphocytes (n = 3) were 90% B26A+, 10% TH21A+ and 10% H4+. Adherent B cell enriched fractions (n = 3) were 10% B26A+, 90% TH21A+ and 90% H4+. The two fluorochrome method was used to simultaneously identify lymphocytes that were sIg+ and MAb+. In these experiments, 92% of all sIg+ cells were H4+. An identical result was obtained for TH21A. 85% of all sIg- cells were B26A+. Using LFC, the mean percentages of sIg+, H4+ and TH21A+ PBL (n = 5) were not significantly different. B26A recognized a significantly greater population of cells, equivalent to the expected percentage of T lymphocytes. LFC also revealed two relatively discrete sizes of B26A+ PBL. The larger population overlapped the size range in which sIg+, H4+, TH21A+ PBL were found. The more numerous smaller B26A+ PBL were in a size range in which few sIg+, H4+ and TH21A+ PBL were found. In a study of MAb reactions with PBL of 185 cows, it was shown that in 92% of the animals H4 and TH21A were positively correlated (r = +.93), when H4 and TH21A were negatively correlated with B26A (r = -.94 and r = -.92, respectively). These correlation coefficients indicate a converse relationship between B26A and both H4 and TH21A. The remaining 8% of the animals were heterogeneous in their expression of the H4 and TH21A markers but not the B26A marker. These results provide strong evidence that: 1) B26A is a pan-T lymphocyte MAb in cattle, 2) a small but significant degree of heterogeneity exists in the expression of the epitopes recognized by H4 and TH21A. However, both MAbs recognize all B lymphocytes of most individuals, and 3) using a variety of immunological methods these three MAbs can now reliably be used to assay bovine T and B lymphocytes.     

Drugs and the liver

The authors discuss the liver's influence on drug disposition in the body and the influence of drugs on the liver. Drug-induced hepatotoxicity with regard to mechanisms and causative agents is discussed, as well as administration of drugs to patients with existing liver disease.