The incidence of nonalcoholic fatty liver disease (NAFLD) has risen along with the ongoing obesity epidemic. Green tea extract (GTE) inhibits intestinal lipid absorption and may regulate hepatic lipid accumulation. The objective of this study was to determine whether GTE protects against hepatic lipid accumulation during the development of NAFLD in an obese mouse model. Five-wk-old ob/ob (obese) mice and their lean littermates (8 mice x genotype(-1) x dietary treatment(-1)) were fed GTE at 0, 1, or 2% (wt:wt) for 6 wk. The body weights of obese mice and lean littermates fed diets containing GTE were 23-25% and 11-20% lower (P < 0.05) than their respective controls fed no GTE. Histologic evaluation showed a significant reduction in hepatic steatosis in GTE-fed obese mice only and histologic scores were correlated with hepatic lipid concentration (r = 0.84; P < 0.05), which was reduced dose dependently by GTE. GTE protected against hepatic injury as suggested by 30-41% and 22-33% lower serum alanine aminotransferase and aspartate aminotransferase activities, respectively. Hepatic alpha-tocopherol was 36% higher in obese mice than lean mice. GTE tended (P = 0.06) to lower hepatic alpha-tocopherol, which was not fully explained by the GTE-mediated reduction in hepatic lipid. Hepatic ascorbic acid was lower in obese mice than in lean mice (P < 0.05) and was unaltered by GTE. Obese mice had lower serum adiponectin than lean mice and this was not affected by GTE. The results suggest that GTE protects against NAFLD by limiting hepatic lipid accumulation and injury without affecting hepatic antioxidant status and adiponectin-mediated lipid metabolism. Further study is underway to define the events by which GTE protects against obesity-triggered NAFLD.

The genomes of novel circoviruses from goose and pigeon, which were isolated using degenerate primer and inverse primer PCR methods, were cloned and sequenced. Comparative nucleotide (nt) sequence analyses showed that the goose circovirus (GCV) and pigeon circovirus (PiCV) possessed genomes which were 1821 and 2037 or 2036 nt, respectively, and which had features in common with the genomes of porcine circoviruses types 1 and 2 (PCV1, PCV2) and psittacine beak and feather disease virus (BFDV), such that they can now be assigned to the genus Circovirus of the family Circoviridae. Common features include the possession of (i) a potential stem-loop/nonanucleotide motif with which the initiation of rolling circle replication of the virus DNA is associated; (ii) two major ORFs, located on the virus (V1 ORF) and complementary (C1 ORF) strands, which encode the replication-associated protein (Rep) and capsid protein, respectively; (iii) high levels of amino acid identity (41.2--58.2%) shared with other circovirus Rep proteins; and (iv) direct/inverted repeat sequences within the putative intergenic region. On the basis of nt and amino acid sequence identities, GCV is substantially less closely related to BFDV than PiCV is to BFDV.

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Bacterial chondronecrosis with osteomyelitis (BCO) in chickens was first reported in 1972 and is now recognized as an important cause of lameness in broiler chickens. Recent systematic studies of causes of lameness in birds reared in Northern Ireland have shown that it was the most common cause of lameness, being present in 17.3% of lame birds. Furthermore, it was also detected in birds presented as ''found dead''. Overall losses in male birds due to BCO were estimated to be 0.75% of all birds placed, which, in addition to welfare concerns, represents considerable economic loss. The disease has been seen in birds ranging from 14 to 70 days of age, but most cases occurred around 35 days old. It is most commonly caused by Staphylococcus aureus, but Escherichia coli, coagulase-negative staphylococci and Enterococcus spp. are sometimes involved, as are, rarely, other bacteria. The lesions are most commonly found associated with the growth plates of long bones, particularly the proximal growth plate of the femur and tibiotarsus, but other bones may also be affected. Since lesions were visible to the naked eye in only 40 to 67% of cases, histological examination is recommended where no lesions are visible macroscopically.As the lesion may be present in only one growth plate, and because histological examination is often not carried out, BCO is almost certainly underdiagnosed. The exact pathogenesis of the condition is unknown, but it is thought that adherence of blood-borne bacteria to exposed cartilage at the tips of metaphyseal blood vessels is fundamental. Under controlled experimental conditions, infection of birds with the immunosuppressive viruses chicken anaemia virus and infectious bursal disease virus increased the incidence of the disease, while restricting feed intake reduced the incidence of disease. S. aureus strains identical to, or closely related to, isolates recovered from naturally occurring cases of the disease (as determined by pulsed-field gel electrophoresis) have been recovered from fluff-debris in hatcheries, and also from the environment of breeding flocks, indicating that infection in the breeding farm and in the hatchery could be an important source of infection. It has also been shown that humans can carry poultry strains of S. aureus on their hands. There is a higher incidence of BCO in birds hatched from floor eggs. Thus, hygiene and management practice on breeder farms and in the hatchery may influence the occurrence of the disease. Bacteraemia is a prerequisite for BCO. Indeed, in some flocks suffering losses due to BCO, there are also losses due to staphylococcal septicaemia. Thus, appropriate treatment of affected flocks should reduce losses due to septicaemia. It should also reduce the occurrence of bacteraemia and the development of further cases of BCO. However, birds in which BCO has already developed, are unlikely to respond to treatment. Control of BCO by vaccination seems unlikely in the short term. Simple bacterins have not been effective and much basic research is needed to id...

This review discusses key factors important in successful experimental reproduction of necrotic enteritis (NE) in chickens, and how these factors can be adjusted to affect the severity of the lesions induced. The critical bacterial factor is the need to use virulent, netB-positive, strains of Clostridium perfringens; disease severity can be enhanced by using netB-positive C. perfringens strains that are also tpeL-positive, by the use of young rather than old broth cultures, and by the number of days of inoculation and the number of bacteria used. Use of cereals rich in non-starch polysaccharides can enhance disease, as does use of animal proteins. Administration of coccidia, including coccidial vaccines, combined with netBpositive C. perfringens, increases the severity of experimentally-induced NE. Dietary manipulation may be less important in coccidia-based models since the latter are so effective. Disease scoring systems and welfare considerations are discussed.