[Statine and endothelium dysfunction in diabetes]. / Statine e disfunzione endoteliale nel diabete.

Diabetes is associated with significant morbidity and mortality in the setting of acute coronary syndromes. Exists a progressive relationship between glucose levels and cardiovascular risk. Hyperglycemy in fact produces endothelial dysfunction recognised to be a key accessory to diabetic microangiopathy and macroangiopathy. Furthermore diabetics present high levels of cholesterol which elevate the risk of CHD. The statins, for their effects, may represent the fit therapy. The beneficial effects of statins may extend beyond improving the lipid profile. There are several proposed mechanisms for event reduction by lipid-lowering therapy, which include improved endothelium-dependent vasodilation, stabilization of atherosclerotic lesions, reduction in inflammatory stimuli, and prevention, slowed progression, or regression of atherosclerotic lesions (pleiotropic effects). Cellular experiments suggest that statins have an impact on endothelial function by preventing oxidized LDL-induced reduction of nitric oxide production and increased nitric oxide synthesis. Statins also impact chronic inflammation by reducing mitogen (PDGF) responsiveness, inhibiting smooth muscle cell proliferation, inhibiting monocyte chemotaxis and migration, and by reducing macrophage protease production. The absolute clinical benefit achieved may be greater in diabetic than in nondiabetic patients with CHD because diabetic patients have a higher absolute risk of recurrent CHD events and other atherosclerotic events.

[Sweet syndrome in a female patient with intestinal multiple lipomas and diverticular disease of the colon]. / Sindrome di Sweet in una paziente con lipomi multipli intestinali e malattia diverticolare del colon.

Sweet's syndrome (SS), or acute febrile neutrophilic dermatosis, is a condition characterized by the sudden onset of fever, leukocytosis, and painful, erythematous, well-demarcated papules and plaques which show dense, neutrophilic infiltrates on histologic examination. Myalgias and arthralgias are common. Although it may occur in the absence of other known disease, SS is often associated with hematologic disease (including leukemia), and immunologic disease (rheumatoid arthritis, inflammatory bowel disease). A case of SS is reported. Furthermore the patient presented multiple intestinal lipomas and diverticular colon disease. The authors, on the ground of recent studies which correlate SS with several digestive system disorders, hypothesize an association between acute febrile neutrophilic dermatosis and patient's intestinal diseases. Treatment with systemic corticosteroids is usually successful.

DISTRIBUTION OF LIPID-SOLUBLE ANTIOXIDANTS IN LIPOPROTEINS FROM HEALTHY SUBJECTS. I. CORRELATION WITH PLASMA ANTIOXIDANT LEVELS AND COMPOSITION OF LIPOPROTEINS.

The concentration of five lipid-soluble antioxidants (gamma- and alpha-tocopherol, lycopene, beta-carotene and ubiquinol-10) was measured in plasma and very low-density, low-density and high-density lipoproteins (VLDL, LDL and HDL) isolated from young healthy normo- cholesterolemic subjects. Alpha-tocopherol was the exclusive antioxidant whose plasma concentration significantly correlated with the absolute concentration of total cholesterol (r =0.541, P<0.001). No correlation was found between plasma concentration and lipoprotein content of alpha-tocopherol and ubiquinol-10, whereas it reached statistically significant values for gamma-tocopherol, lycopene and beta-carotene. The alpha-tocopherol content in VLDL and HDL, but not in LDL, was strictly associated with the relative abundance of cholesterol and phospholipids in the lipoprotein particles. Moreover, the difference between alpha-tocopherol concentration in VLDL and LDL appeared to be strictly related to the differences in cholesterol, phospholipids and triglycerides. The percent distribution of the total plasma pool of antioxidant in each lipoprotein class revealed that gamma- and alpha-tocopherol were roughly equally distributed in LDL and HDL. On the other hand, lycopene, beta-carotene and ubiquinol-10 were preferentially sequestered in LDL. Finally, the absolute and relative concentration of alpha-tocopherol, but not that of other antioxidants, in HDL exhibited a statistically significant correlation with plasma HDL/LDL cholesterol ratio. These findings indicate that: (i) plasma concentrations of major lipid-soluble antioxidants are not always predictive of their levels in lipoproteins and that, within individual lipoprotein classes, (ii) the lipid composition, metabolism and relative plasma concentration may significantly affect their abundance. 2000 Academic Press@p$hr Copyright 2000 Academic Press.

DISTRIBUTION OF LIPID-SOLUBLE ANTIOXIDANTS IN LIPOPROTEINS FROM HEALTHY SUBJECTS. II. EFFECTS OF IN VIVO SUPPLEMENTATION WITH alpha-TOCOPHEROL.

The effects of orally supplemented dl -alpha-tocopherol on the plasma concentration of lipid-soluble antioxidants and their distribution in very-low-density, low-density and high-density lipoproteins (VLDL, LDL and HDL) was investigated in a cohort of control normocholesterolemic adult subjects receiving 600 mg alpha-tocopherol daily for 2 weeks. This regimen did not modify the plasma lipid profile (total, LDL and HDL cholesterol and triglycerides) and chemical composition of VLDL, LDL and HDL. Plasma concentration of alpha-tocopherol increased from 19.44+/-4.77 to 38.03+/-9.06 µm and this was associated with slight decrease in the concentration of gamma-tocopherol from 1.27+/-0.97 to 0.99+/-1.17 µm, without any significant changes of either lycopene and beta-carotene. Qualitatively similar changes were found in VLDL, LDL and HDL but the net increase of alpha-tocopherol in plasma did not correlate with the increase in alpha-tocopherol content in any of the lipoprotein types. Following supplementation, the percentage of total plasma alpha-tocopherol pool carried by VLDL increased from 20.97+/-6.07% to 33.57+/-6.97%, whereas it decreased from 41.85+/-7.02% to 36.36+/-5.69% in the case of LDL and from 37.17+/-6.04% to 30.05+/-4.88% in the case of HDL. The absolute and relative enrichment of alpha-tocopherol in either VLDL and LDL did not exhibit any statistically relevant correlation with the chemical composition of these lipoproteins in the different subjects investigated. On the other hand, the amount of alpha-tocopherol enriching the HDL particles was inversely related to the relative abundance of protein (r =0.449;P<0.05) and directly to the phospholipid/protein ratio (r =0.480, P<0.05). 2000 Academic Press@p$hr Copyright 2000 Academic Press.

The kinetics of copper-induced LDL oxidation depend upon its lipid composition and antioxidant content.

Copper promotes oxidation of human low-density lipoprotein (LDL) through molecular mechanisms that are still under investigation. We employed native human LDL, phospholipid-containing delipidated LDL ghosts, or trilinolein-reconstituted, phospholipid-containing LDL to investigate both LDL oxidation and the associated process of copper reduction. Both LDL ghosts and trilinolein-reconstituted LDL were devoid of antioxidants and were extremely susceptible to AAPH-induced oxidation but, paradoxically, were rather resistant to copper-mediated oxidation. The dynamic reduction of Cu(II) to Cu(I) was quantitatively decreased in LDL ghosts and in trilinolein-reconstituted LDL, also lacking the initial rapid reduction and the subsequent inhibition phases, due to the absence of endogenous antioxidants. Conversely, the rate of copper reduction was linear and likely due to lipid peroxides, either already present or formed during copper-induced oxidation. We suggest that copper undergoes redox transitions in LDL by utilizing reducing equivalents originating from endogenous antioxidants and/or from lipid peroxides in the LDL lipid core.

Distribution of lipid-soluble antioxidants in lipoproteins from healthy subjects. I. Correlation with plasma antioxidant levels and composition of lipoproteins.

The concentration of five lipid-soluble antioxidants (gamma- and alpha-tocopherol, lycopene, beta-carotene and ubiquinol-10) was measured in plasma and very low-density, low-density and high-density lipoproteins (VLDL, LDL and HDL) isolated from young healthy normo- cholesterolemic subjects. Alpha-tocopherol was the exclusive antioxidant whose plasma concentration significantly correlated with the absolute concentration of total cholesterol (r =0.541, P<0.001). No correlation was found between plasma concentration and lipoprotein content of alpha-tocopherol and ubiquinol-10, whereas it reached statistically significant values for gamma-tocopherol, lycopene and beta-carotene. The alpha-tocopherol content in VLDL and HDL, but not in LDL, was strictly associated with the relative abundance of cholesterol and phospholipids in the lipoprotein particles. Moreover, the difference between alpha-tocopherol concentration in VLDL and LDL appeared to be strictly related to the differences in cholesterol, phospholipids and triglycerides. The percent distribution of the total plasma pool of antioxidant in each lipoprotein class revealed that gamma- and alpha-tocopherol were roughly equally distributed in LDL and HDL. On the other hand, lycopene, beta-carotene and ubiquinol-10 were preferentially sequestered in LDL. Finally, the absolute and relative concentration of alpha-tocopherol, but not that of other antioxidants, in HDL exhibited a statistically significant correlation with plasma HDL/LDL cholesterol ratio. These findings indicate that: (i) plasma concentrations of major lipid-soluble antioxidants are not always predictive of their levels in lipoproteins and that, within individual lipoprotein classes, (ii) the lipid composition, metabolism and relative plasma concentration may significantly affect their abundance.

Distribution of lipid-soluble antioxidants in lipoproteins from healthy subjects. II. Effects of in vivo supplementation with alpha-tocopherol.

The effects of orally supplemented dl -alpha-tocopherol on the plasma concentration of lipid-soluble antioxidants and their distribution in very-low-density, low-density and high-density lipoproteins (VLDL, LDL and HDL) was investigated in a cohort of control normocholesterolemic adult subjects receiving 600 mg alpha-tocopherol daily for 2 weeks. This regimen did not modify the plasma lipid profile (total, LDL and HDL cholesterol and triglycerides) and chemical composition of VLDL, LDL and HDL. Plasma concentration of alpha-tocopherol increased from 19.44+/-4.77 to 38. 03+/-9.06 microm and this was associated with slight decrease in the concentration of gamma-tocopherol from 1.27+/-0.97 to 0.99+/-1.17 microm, without any significant changes of either lycopene and beta-carotene. Qualitatively similar changes were found in VLDL, LDL and HDL but the net increase of alpha-tocopherol in plasma did not correlate with the increase in alpha-tocopherol content in any of the lipoprotein types. Following supplementation, the percentage of total plasma alpha-tocopherol pool carried by VLDL increased from 20. 97+/-6.07% to 33.57+/-6.97%, whereas it decreased from 41.85+/-7.02% to 36.36+/-5.69% in the case of LDL and from 37.17+/-6.04% to 30.05+/-4.88% in the case of HDL. The absolute and relative enrichment of alpha-tocopherol in either VLDL and LDL did not exhibit any statistically relevant correlation with the chemical composition of these lipoproteins in the different subjects investigated. On the other hand, the amount of alpha-tocopherol enriching the HDL particles was inversely related to the relative abundance of protein (r =0.449;P<0.05) and directly to the phospholipid/protein ratio (r =0.480, P<0.05).

When and why a water-soluble antioxidant becomes pro-oxidant during copper-induced low-density lipoprotein oxidation: a study using uric acid.

The inclusion of uric acid in the incubation medium during copper-induced low-density lipoprotein (LDL) oxidation exerted either an antioxidant or pro-oxidant effect. The pro-oxidant effect, as mirrored by an enhanced formation of conjugated dienes, lipid peroxides, thiobarbituric acid-reactive substances and increase in negative charge, occurred when uric acid was added late during the inhibitory or lag phase and during the subsequent extensive propagation phase of copper-stimulated LDL oxidation. The pro-oxidant effect of uric acid was specific for copper-induced LDL oxidation and required the presence of copper as either Cu(I) or Cu(II). In addition, it became much more evident when the copper to LDL molar ratio was below a threshold value of approx. 50. In native LDL, the shift between the antioxidant and the pro-oxidant activities was related to the availability of lipid hydroperoxides formed during the early phases of copper-promoted LDL oxidation. The artificial enrichment of isolated LDL with alpha-tocopherol delayed the onset of the pro-oxidant activity of uric acid and also decreased the rate of stimulated lipid peroxidation. However, previous depletion of alpha-tocopherol was not a prerequisite for unmasking the pro-oxidant activity of uric acid, since this became apparent even when alpha-tocopherol was still present in significant amounts (more than 50% of the original values) in LDL. These results suggest, irrespective of the levels of endogenous alpha-tocopherol, that uric acid may enhance LDL oxidation by reducing Cu(II) to Cu(I), thus making more Cu(I) available for subsequent radical decomposition of lipid peroxides and propagation reactions.

Non specific serological reactions in the diagnosis of bovine brucellosis: experimental oral infection of cattle with repeated doses of Yersinia enterocolitica O:9.

Eight heifers were orally infected with 4 x 10(9) colony forming units of a field cattle strain of Yersinia enterocolitica O:9 in a capsule, 5 days a week, for about 9 weeks (day 0-day 64 (D0-D64). The faecal shedding of Y. enterocolitica O:9 began on D5 for seven out of the eight challenged cattle with a high level of excretion during the first month, followed by a decrease till the day of slaughter (D76). Y. enterocolitica O:9 was not isolated from organs collected at slaughter. No clinical symptoms were observed. Hyperplasia of intestinal lymph formations was the sole microscopic lesions observed. Five animals showed a serological reaction against Brucella antigens in at least one of the following tests: Rose-Bengal test, complement fixation test, tube agglutination test or indirect ELISA (iELISA) tests. Only one animal showed a high level of serological response and a positive reaction in the dithiothreitol-microagglutination test. The observed variability in terms of individual sensitivity to the Y. enterocolitica O:9 infection is in agreement with the low individual prevalence rate and the transient serological reaction and faecal Y. entercolitica O:9 shedding observed in herds showing false positive serological reactions in brucellosis.

[TTV: a new hepatitis virus? Transfusion-transmitted virus]. / TTV: un nuovo virus epatitico?

Following the discovery of hepatitis C virus (HCV), it was clear that a proportion of cases with acute and chronic hepatitis are still negative for all known viral markers, which prompted investigations to search for new hepatitis agents. In 1997 investigators in Japan isolated a DNA clone of a novel human virus using a representation difference analysis from serum samples from a patient (TT) with post-transfusion hepatitis of unknown etiology and designated TTV for transfusion-transmitted virus. TTV DNA is common in populations at increased risk for infection with hemophilia or maintenance hemodialysis and abusers of intravenous drugs. As a nonenveloped virus with a linear, single stranded genomic DNA, TTV resembles the Parvoviridae among known animal viruses. TTV has been reported in association with post-transfusion and acute and chronic hepatitis of unknown etiology. Phylogenetic analysis indicated six different genotypes of TTV with distinct subtypes [correction of sottotypes]. Viral DNA can be detected in plasma but also in liver tissue of infected subjects, suggesting that it is hepatotropic. TTV can be transmitted parenterally by blood and blood products and probably also non-parenterally by a fecal-oral route. TTV DNA is present in a large proportion of patients with different forms of non-A-G hepatitis. A new simple genotyping assay based on a restriction fragment length polymorphism of TTV was developed. This system will provide the framework for future detailed epidemiological and clinical investigations.

[The Brugada syndrome. A predicted sudden juvenile death]. / La sindrome di Brugada. Una morte giovanile improvvisa preannunciata.

This review deals with the clinical, basic and genetic aspects of recently highlighted form of idiopathic ventricular fibrillation known as the Brugada syndrome. The available data suggest that the Brugada syndrome is a primary electrical disease resulting in abnormal electrophysiological activity in the right ventricular epicardium. Diagnosis is based on the presence of an ST elevation in the anteroseptal territory and a right branch block. No underlying dysarrhythmic condition or arrhythmogenic heart disease can be detected. The available data suggest that less of the action potential dome in the right ventricular epicardium but not endocardium underlies the ST segment elevation seen in the Brugada syndrome and that electrical heterogeneity within right ventricular epicardium leads to the development of closely coupled premature ventricular contractions via a phase 2 reentrant mechanism that then precipitates ventricular tachycardia/ventricular fibrillation. Brugada syndrome is a recently discovered hereditary condition with a probably underestimated prevalence. Systematic family studies have demonstrated an autosomal dominant inheritance. The characteristic electrocardiographic anomalies can be transitory and may be unmasked by sensitization tests. The only currently treatment is the implantable defibrillator programmed to prevent sudden death by ventricular fibrillation and it is indicated in symptomatic patients and should be considered in asymptomatic patients in whom ventricular tachycardia/ventricular fibrillation is inducible by electrophysiologic study.

[Syndrome of increased idiopathic capillary permeability (Clarkson's syndrome)]. / Sindrome da aumentata permeabilità capillare idiopatica. (Sindrome di Clarkson).

Idiopathic systemic capillary leak syndrome (Clarkson's disease) is characterized by recurring attacks or increased capillary permeability, resulting in severe hypovolemic shock due to plasma extravasation from the intravascular compartment. Additional laboratory features include association with a monoclonal gammopathy, extreme hemoconcentration and hypoalbuminemia. The underlying cause is not known and there have been fewer than 40 cases reported. It affects people aged 30-40 years and has a high mortality, with only six of 25 patients surviving for more than 5 years. Marked thirst is noted early in the attack and profound muscle weakness, anorexia; nausea, and vomiting are present in all patients, especially so during the course of an attack. Generally, oedema appeared several hours or days before the onset of shock. The total duration of illness varied from six months to seven years. An unknown trigger causes a temporary increase in the macromolecular permeability in the capillary bed of skeletal muscle and connective tissue. The syndrome of rhabdomyolysis includes myalgia, swelling and weakness of the involved muscle groups, pigmenturia, and leakage of myoglobin and CK into the serum. Different treatments have been tried, including plasmapheresis, steroids, epoprostenol, salbutamol and Gingko biloba extract with success in some cases. Treatment with corticosteroids should be considered for prevention of attacks in the systemic capillary leak syndrome.

[The Alice in Wonderland syndrome]. / La sindrome di Alice nel paese delle meraviglie.

The "Alice in Wonderland syndrome includes an array of symptoms involving altered perception of shape (meta-morphopsia) of objects or persons who appear to be smaller (micropsia) or larger (macropsia) than normal, of impaired sense of passage of time, of zooming of the environment. This unusual neurological picture which can be confused with psychosis or drug intoxication has been found to accompany cerebral lesions mainly temporo-occipital or parietal-occipital temporal epilepsy and migraine. Todd gave the syndrome its literary name in his report in 1955, describing a singular group of symptoms closely associated with migraine and epilepsy. However the first description of the condition was made by Lippman in 1952. This syndrome is so called because of the resemblance of its symptoms to the fluctuations in size and shape that plague the main character in Lewis Carrol's 1865 novel Alice in Wonderland. Cases of "Alice in Wonderland" syndrome have been described associated with infectious mononucleosis. In each clinical case, the classical infectious mononucleosis symptoms and diagnosis followed the onset of visual aberration. Nuclear medicine techniques are able to demonstrate changes in cerebral perfusion and may be used to detect abnormal cerebral areas in patients with AIWS.

Different mechanisms are progressively recruited to promote Cu(II) reduction by isolated human low-density lipoprotein undergoing oxidation.

The kinetics of Cu(II) reduction and its relationship to the process of low density lipoprotein (LDL) oxidation were investigated in isolated human LDL incubated with CuSO4 by using the Cu(I) chelator and indicator dye bathocuproine disulfonate (BC). The inclusion of BC in the incubation medium containing isolated LDL and different concentrations of CuSO4 revealed a biphasic kinetics of Cu(II) reduction consisting of an early phase followed by a plateau phase and a subsequent extensive reduction phase. The amount of Cu(I) formed during the early phase, as well as the rate of its generation, were strictly dependent on both the level of Cu(II) available (saturation was observed at 20 and 50 microM CuSO4) and the concentration of alpha-tocopherol within native LDL particles. Artificial enrichment of LDL with different concentrations of alpha-tocopherol led to a parallel increase of both the amount of Cu(II) reduced and the rate of reduction. The late phase of Cu(II) reduction was strictly related to the availability of copper but was largely independent from alpha-tocopherol. Neither the amount of Cu(I) generated nor the rate of generation were saturated at concentrations of copper up to 100 microM. Comparable results were obtained by adding BC at different time-points to the LDL-copper mixture, in order to measure at the same time-points both the true rate of Cu(II) reduction and the generation of TBARS during the dynamic process of LDL oxidation. The rate of Cu(II) reduction was already high during the lag-phase of the LDL oxidation profile and progressively decreased as alpha-tocopherol concentration decreased. The subsequent increase in the rate of Cu(II) reduction paralleled the formation of TBARS during the extensive LDL oxidation phase. These results suggest that different mechanisms of Cu(II) reduction, namely alpha-tocopherol-dependent and independent (likely lipid peroxide-dependent), are progressively recruited during copper-promoted LDL oxidation.

VH gene expression in hairy cell leukaemia.

Hairy cells are characterized by their typical morphology and expression of specific surface antigens. Although their B-cell origin is now confirmed, their exact position in B-cell development remains unclear. To better define the origin of hairy cells, we analysed the immunophenotype and the Ig VH nucleotide sequence of seven cases of hairy cell leukaemia (HCL). Six of them were typical HCL and the remaining case corresponded to a variant HCL. Analysis of sequenced VH genes revealed that the VH1 family was used in one case, VH2 in one, VH3 in two, VH4 in two and VH5 in one. No preferential usage of VH genes was observed in this small series. In five cases high rates of somatic mutations were observed, with a predominance of mutations and replacements in CDR regions for three. indicating that these cells originate from cells that have been exposed to the hypermutation mechanism. The distribution of mutations in our small series provides some evidence of a selective mutational process.

Cu(I) availability paradoxically antagonizes antioxidant consumption and lipid peroxidation during the initiation phase of copper-induced LDL oxidation.

The incubation of isolated human low-density lipoprotein (LDL) with Cu(II) promoted extensive oxidation of both the lipid and protein moieties of the lipoprotein particle. When the Cu(II) to LDL molar ratio was equal or higher than 50, the removal of Cu(I) formed by the contemporary presence of the Cu(I) chelator bathocuproine disulphonate (BC) markedly accelerated the formation of end-products of lipid peroxidation. Moreover, the initial rate of Cu(II)-induced consumption of either endogenous antioxidants in LDL or free alpha-tocopherol in suspension was increased in the presence of BC, thus indicating that the continuous removal of Cu(I) enhanced both antioxidant consumption and LDL oxidation promoted by copper. Furthermore, the direct addition of Cu(I), together with Cu(II), to a suspension of isolated LDL efficiently delayed the onset of extensive lipid peroxidation and decreased the rate of antioxidant consumption. The latter effect, however, was detectable exclusively on LDL-associated alpha-tocopherol and not on alpha-tocopherol in suspension, thus suggesting that the competition between Cu(I) and Cu(II) was taking place at discrete sites associated with the LDL particle. Finally, the inclusion of Cu(I) in the incubation medium of LDL already undergoing extensive peroxidation did not inhibit but rather markedly stimulated the rate of peroxidation. Although apparently in contrast with the common view that Cu(I) and not Cu(II) is the real trigger species of LDL oxidation in the copper model, the results reported here indicate that the availability of Cu(I) during the initiation phase of LDL oxidation promoted by copper antagonizes both antioxidant consumption and the onset of extensive oxidation.

[Primary dilated cardiomyopathy]. / Cardiomiopatia dilatativa primitiva.

Recent advances in etiopathogenesis and natural history of idiopathic dilated cardiomyopathy are presented. The clinical and instrumental diagnosis and therapy are also reported.

The Brucellin skin test as a tool to discriminate false positive serological reactions in bovine brucellosis.

Three experiments were performed in order to assess the diagnostic value of the Brucellin allergic skin test (AST) in a brucellosis false positive serological reactions (FPSR) context. First, 1259 cattle from 20 Brucella-free herds in a FPSR area were tested twice with AST to estimate its specificity. Secondly, AST and serological tests (complement fixation test [CFT], tube agglutination test, dithiothreitol-microagglutination test and ELISA) sensitivities were evaluated on 111 cattle positive to the Rose Bengal test (RBT) belonging to 15 Brucella-infected herds. Thirdly, AST was used in a field trial to discriminate FPSR from true brucellosis reactions. AST specificity in non-vaccinated cattle was very high (99.83%; confidence interval 95% [CI95%]: 99.67-99.96%). Skin thickening 72 h post-injection was significantly higher on vaccinated cattle (1.42 vs 0.15 mm). In this sub-population, AST specificity decreased significantly to 78% (CI95%: 68-87%). Individual sensitivity of AST relative to Rose Bengal test was 64% (CI95%: 54-72%), while all infected herds were AST positive (n = 15). When associated with CFT, it detected 95% (CI95%: 90-98%) of the infected cattle. These results were consistent with the field trial. In a FPSR context, AST was more specific than RBT or CFT. Therefore, this test could be used at herd level as a confirmation test, on cattle non vaccinated against brucellosis.

False positive serological reactions in bovine brucellosis: evidence of the role of Yersinia enterocolitica serotype O:9 in a field trial.

To investigate the epidemiology of false positive serological reactions (FPSR) in bovine brucellosis, 1259 bovines from 20 herds were sampled on three successive occasions during the winter of 1993-1994 in an area where the herd prevalence rate of FPSR was high. Serum samples were examined by classical brucellosis serological tests (Rose Bengal and complement fixation) and faeces were cultured for the presence of Yersinia enterocolitica O:9. Thirty-nine bovines expressed at least one positive serological reaction during the study. In the herds with FPSR during the 1993-1994 annual brucellosis surveillance campaign, the specificity of the brucellosis serological tests varied significantly from December to March (97.0% to 99.1%). Y enterocolitica O:9 was isolated from 42 bovines but only three of them showed a positive serological response during the study. Y enterocolitica O:9 isolation rates also decreased with time. Young animals and animals having demonstrated FPSR in the past had a greater risk of having a FPSR. Older animals, which rarely showed FPSR, could form a reservoir for Y enterocolitica O:9. While isolation of Y enterocolitica O:9 was not linked to presence of FPSR and conversely, the FPSR phenomenon should be considered, either at the herd level or at the individual level. This work reinforces the link, at least partial, between FPSR and infection by Y enterocolitica O:9.

Efficacy of different Rose Bengal and complement fixation antigens for the diagnosis of Brucella melitensis infection in sheep and goats.

Fifteen different Rose Bengal antigens showed large differences with respect to pH, cell concentration and agglutination with the international standard anti-Brucella abortus serum, demonstrating the lack of international standardisation. Their sensitivity and specificity, compared with that of the complement fixation test, were evaluated for the diagnosis of B melitensis infection in culture-positive sheep, brucella-free ewes, and sheep and goats belonging to field flocks under different epidemiological conditions. All the Rose Bengal antigens and the complement fixation test had 100 per cent specificity when testing brucella-free sheep or animals belonging to flocks in unvaccinated brucellosis-free areas, but there were large differences in sensitivity between the Rose Bengal antigens with sera from culture-positive sheep or from animals belonging to infected flocks. When using the most sensitive antigen, no difference was observed in Rose Bengal sensitivity between animals infected with either biovar 1 or biovar 3 of B melitensis. The relationship between the sensitivity of the Rose Bengal antigens and cell concentration was unclear, but their sensitivity was related to the standardisation of the antigens with the international standard serum. The complement fixation test was less sensitive than the Rose Bengal test when testing culture-positive sheep. When testing sera from animals belonging to infected flocks with antigens standardised according to European Union rules, no great differences were observed in the sensitivities of the two tests. However, great differences in sensitivity between the Rose Bengal antigens were observed with sera from animals belonging to flocks with low levels of prevalence.(ABSTRACT TRUNCATED AT 250 WORDS)