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Biomedical subjects

R G Batey

Publications and source records attributed to R G Batey.

At least 55 records · Page 3Linked to original sources

Hepatitis B in Australia: determinants of intrafamily spread.

Strategies for the control of hepatitis B virus (HBV) infection rely on information about the modes of spread and the numbers of 'at risk' individuals in particular community subgroups. This study prospectively examined 377 family and household contacts of 145 patients with HBV infection to determine the incidence of and factors determining intrafamily spread. Two hundred and forty were contacts of 68 Asian patients and 137 were contacts of 77 Caucasian patients. Serological examination of all contacts demonstrated that 161 (43%) had HBV markers including 60 (16%) who were HBsAg positive. HBV transmission within families was greater if the index case was Asian rather than Caucasian (p less than 0.001), had an HBsAg positive mother rather than an HBsAg positive father (p less than 0.01), was HBeAg positive rather than HBeAg negative (p less than 0.002), and had chronic rather than acute HBV infection (p less than 0.001). However birthplace, family size, and the activity of the liver disease of the index case did not influence HBV transmission. Within Asian families, the risk of non-sexual and non-vertical transmission of hepatitis B appeared to be as high as 18% and continued after the first three years of life. It is concluded that hepatitis B prevention programmes should include vaccination of families of chronic HBV carriers, particularly those from endemic regions such as Asia.

Adolescent↗

Factors affecting the yield of viable cells of Corynebacterium pseudotuberculosis in a liquid medium.

Growth of Corynebacterium pseudotuberculosis in an undefined liquid medium was studied with the aim of obtaining uniform, single-cell suspensions of the organism suitable for experimental infection. Adequate yields of viable cells were shown to be dependent on a fermentable substrate and a buffering system in a medium containing Tween 80. The development of Nutrient Tween 80 Broth for the culture of C. pseudotuberculosis is considered to be a significant advance particularly for studies involving animal inoculation.

Animals↗

Aspects of pathogenesis in a mouse model of infection by Corynebacterium pseudotuberculosis.

A new medium, nutrient tween 80 broth (NTB) was utilised to achieve improved cultivation of Corynebacterium pseudotuberculosis. Twenty four hour NTB cultures were used for cutaneous and intraperitoneal infection of mice. The intraperitoneal administration of heterologous protein, liquid paraffin or thioglycollate prior to intraperitoneal challenge caused enhanced multiplication of the organism although this could be prevented by modifying host response. Pretreatment of skin with thioglycollate enabled cutaneous infection to be consistently achieved. The progress of lesions in skin and viscera is described. Immunisation of the mice was effected by both intraperitoneal and cutaneous routes of inoculation, the latter being particularly useful because it did not lead to residual lesions of viscera. Immunity was expressed by a failure of organisms to localise at secondary sites although infection of primary sites in skin or peritoneal cavity occurred, apparently at a reduced level. The relevance of these findings to the natural disease of sheep is discussed.

Agglutination↗

Prevalence and distribution of caseous lymphadenitis in feral goats.

A total of 2,920 feral goats from pastoral areas of Western Australia were examined and the prevalence of caseous lymphadenitis was estimated to be 7.8 +/- 0.9% in goats presented for slaughter. Head, body and visceral lesions were present in 49.3%, 46.7% and 12.3% of affected goats, respectively. A comparison with previously reported data from sheep has been made and significant differences are discussed. Lung lesions were relatively uncommon in goats, whereas the distribution of carcase lesions was similar between the species. Multiple lesions appear to be less common in goats than in sheep.

Age Factors↗

Pathogenesis of caseous lymphadenitis in sheep and goats.

The progress of caseous lymphadenitis in sheep and goats is described as involving primary wound infection, lymphatic and haematogenous dissemination, and secondary infection of lymph nodes and various visceral organs. This is followed by elimination or containment of infection, the latter being represented by the characteristic caseous lesions. Resistance to infection is complex involving components of both the specific and non-specific host response. The role of these in pathogenesis is discussed. Bacterial factors including the phospholipase exotoxin and cytotoxic lipid contribute to pathogenesis at a local level with little likelihood of systemic effect in the natural disease. In a disease such as caseous lymphadenitis, lesion site, size or number do not indicate severity of disease but rather, reflect the ability of the host to mount a cellular response to infection.

Animals↗

Frequency and consequence of caseous lymphadenitis in sheep and lambs slaughtered at a Western Australian abattoir.

A total of 8,711 sheep in 3 distinct age/sex groups were examined to determine for occurrence and extent of caseous lymphadenitis after slaughter at a major Western Australian abattoir. An adaptation of current mean inspection procedures to provide a numerical weighted evaluation according to number, site, and size of lesions was used to determine extent of involvement. Frequency in slaughter populations was estimated to be 3.4 +/- 0.6% for lambs, 41.8 +/- 3.9% for mixed-age rams, and 53.7 +/- 1.5% for adult ewes at 95% confidence intervals. The results confirmed that frequency increased with age, but also revealed increases in extent of involvement and occurrence of visceral lesions, particularly in association with lesions of the body. Nevertheless, lesions occurred more frequently in the body than in the viscera. However, the mean visceral involvement was greater than mean body involvement in all groups, and the ratio was found to be more or less constant. Visceral involvement was found to be more extensive in rams than in ewes. Difficulties associated with complexity of current inspection procedures were also recorded. The relevance of these findings to pathogenesis and postmortem disposition after slaughter is discussed. It is suggested that current postmortem inspection criteria should be reevaluated.

Aging↗

Erythrocyte ferritin content in idiopathic haemochromatosis and alcoholic liver disease with iron overload.

The erythrocyte ferritin content was measured in patients with either idiopathic haemochromatosis or alcoholic liver disease and iron overload to define its value as a marker for an excess of tissue iron. The mean erythrocyte ferritin content in patients with untreated idiopathic haemochromatosis was increased 60-fold and fell with phlebotomy. After phlebotomy many patients had an increased red cell ferritin content despite normal serum ferritin concentrations. That this reflected persistent iron overload with inadequate phlebotomy was suggested by the higher serum iron concentrations, percentage transferrin saturation, and urinary excretion of iron after administration of desferrioxamine, together with a lower annual iron loss by phlebotomy in this group compared with patients with treated disease and normal red cell ferritin content. The mean erythrocyte ferritin content in patients with alcoholic liver disease and iron overload was increased only sevenfold, and the ratio of erythrocyte to serum ferritin clearly discriminated these patients from those with idiopathic haemochromatosis. The determination of erythrocyte ferritin content is a useful non-invasive test for diagnosing idiopathic haemochromatosis, monitoring the effect of phlebotomy in this disorder, and distinguishing patients with this disorder from those with alcoholic liver disease with iron overload.

Adult↗

Effect of iron stores on hepatic metabolism of transferrin-bound iron.

Hepatic and splenic accumulation and hepatic subcellular distribution of iron from a tracer dose of purified 59Fe-labeled transferrin were studied in normal, iron-deficient, iron-loaded, and pregnant rats. Hepatic and splenic 59Fe content was determined at varying intervals and the subcellular distribution then studied. In normal rats hepatic accumulation of 59Fe was biphasic with 9-10% of the dose present in the liver in the first 2 h postinjection, followed by a plateau of 4 h and a second rise to 20-25% at 16-18 h. During iron deficiency, 5-6% of the dose accumulated in the liver in 2 h and remained at this level. Iron loading resulted in a rapid accumulation of 17% of the dose at 6 h, and the normal plateau was absent. Splenic iron accumulation was similar in the normal and iron-loaded groups with approximately 3% of the dose present in the spleen over the 7-day study. Iron deficiency resulted in a threefold increase in splenic iron content to 10% of the dose at 1 h postinjection. Hepatic and splenic iron accumulation was markedly depressed in the pregnant group. Subcellular distribution studies showed that the 59Fe moved rapidly into ferritin in all groups and was not at any time associated with either lysosomes or mitochondria. These studies present further physiological data of the effects of differing iron states on hepatic and splenic iron accumulation.

Animals↗

Alcohol and the liver. A review of pathogenetic mechanisms and newer treatment approaches.

A great deal has been learned about the hepatotoxicity of ethanol in the past two decades. Possible mechanisms of hepatic damage have been elucidated in animal and human experimental situations, and much has been learned about those factors which may hasten or facilitate the production of liver injury. All the answers to the difficult question of individual susceptibility have yet to be provided. Some progress has been made in the management of alcohol related liver injury, but again much more needs to be made. Abstinence remains the cornerstone of therapy in patients with alcoholic hepatitis and cirrhosis. The roles of colchicine, amino-acid therapy and propylthiouracil are still being determined. The most important message for the physician in 1983 remains: Prevent alcohol related liver disease.

Alcoholism↗

Hepatitis and haemophilia therapy in Australia.

243 Australian haemophiliacs have been studied retrospectively over 4 1/2 years to assess the effect of treatment products on liver function and to determine the frequency of hepatitis-B markers in these patients. Commercial blood products are not used in Australia, and the patients were treated with products of blood from unpaid donors screened for hepatitis B surface antigen. Cryoprecipitate was the major treatment product, and only small amounts of factor VIII and IX concentrates were used. Despite the use of blood products obtained from entirely voluntary blood donors and the frequent use of single-donor packs of cryoprecipitate, markers of viral hepatitis were common in these haemophiliacs. Antibody to hepatitis B surface antigen was detected in 63% of the patients, and there were 66 cases of non-A, non-B hepatitis during the study. 29 of these episodes persisted for longer than 6 months. 13 patients (5.4%) had hepatitis B during the study; 2 patients remained HBsAg-positive for longer than 6 months. Abnormal serum aminotransferase levels were found in 34% of the patients; in 8% of patients these abnormalities persisted for more than 6 months.

Adolescent↗

Properties and hepatic metabolism of non-transferrin-bound iron.

These experiments have examined the physical properties and the hepatic uptake of non-transferrin-bound iron, a fraction found in the serum of untreated primary hemochromatosis patients. Ultrafiltration, polyacrylamide gel electrophoresis, and TLC have demonstrated the non-transferrin-bound iron complex to have a molecular weight less than 1000 and to be distinct from free iron and amino acid iron complexes. Hepatic iron uptake from serum containing non-transferrin-bound iron was significantly higher than from the same serum sample from which the abnormal iron had been removed. Non-transferrin-bound iron entering the liver was localized to the lysosomal fraction in the first hour and was subsequently incompletely incorporated into ferritin. The results demonstrated an abnormal uptake of this iron fraction by the liver and suggest that the abnormal serum fraction may contribute to tissue damage by entering the lysosomes.

Animals↗

A non-transferrin-bound serum iron in idiopathic hemochromatosis.

The nature of iron in the serum of patients with idiopathic hemochromatosis has been studied utilizing an isotope labeling method and results have been compared with those from normal individuals and patients with other forms of liver disease. Between 2 and 4% of a tracer dose of 59Fe added to normal serum was retained by DEAE Sephadex and has been designated non-transferrin-bound. Alcoholic liver disease, chronic active hepatitis, and iron deficiency have no effect on this fraction. In idiopathic hemochromatosis 34.6 +/- 3.9% of the added iron was not bound to transferrin at diagnosis, representing approximately 700 microgram Fe/liter serum. Treatment lowers this fraction before serum iron concentration falls to normal. The majority of the non-transferrin-bound iron is of low molecular weight and is not bound to albumin. The presence of this fraction may contribute significantly to the development of tissue siderosis.

Binding Sites↗