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Biomedical subjects

R L Reece

Publications and source records attributed to R L Reece.

At least 19 recordsLinked to original sources
PubMed2003

An outbreak of highly pathogenic avian influenza in Australia in 1997 caused by an H7N4 virus.

In November of 1997 an outbreak of highly pathogenic avian influenza occurred near the town of Tamworth, in northern New South Wales, Australia. The viruses isolated from chickens on two commercial chicken farms were identified as H7N4 viruses, with hemagglutinin cleavage site amino acid sequences of RKRKRG and intravenous pathogenicity indices of 2.52 and 2.90, respectively. A virus with an identical nucleotide sequence, but with an intravenous pathogenicity index of 1.30, was also isolated from cloacal swabs collected from asymptomatic emus kept on a third property.

Animals↗
PubMed2002

Spironucleosis in Australian king parrots (Alisterus scapularis).

OBJECTIVE: To describe a syndrome of wasting, diarrhoea and mortality in Australian king parrots (Alisterus scapularis). DESIGN: Field observations and laboratory examinations. Procedure Pathological examinations were performed on 50 Australian king parrots with wasting and diarrhoea. Wet preparations of intestinal contents were examined by light microscopy. Tannins were extracted from acorns (Quercus sp) and tested for toxicity in mice. CLINICAL SIGNS AND EPIDEMIOLOGY: A syndrome of wasting, diarrhoea and mortality was observed in wild juvenile Australian king parrots in eastern Australia from 1984 to 2000. Sporadic cases and outbreaks of disease occurred from May to September in New South Wales, the Australian Capital Territory and Victoria. Outbreaks in the Australian Capital Territory in 1990 and 1991 were associated with parrots congregating to feed on acorns. Most affected birds failed to respond to treatment with dimetridazole and died 1 to 14 days after hospitalisation. Selected cases recovered following treatment with metronidazole. PATHOLOGY: Affected birds were emaciated, with faecal matting of feathers around the cloaca and yellow-green fluid, foamy intestinal contents. Abundant motile Spironucleus trophozoites were observed in wet preparations of faeces of clinically affected birds and intestinal contents of birds examined within 1 h of death. Protozoa were detected histologically in crypts of Lieberkühn in the intestine in association with exudation of mucus (catarrhal enteritis) or lymphoplasmacytic enteritis. Toxicology Tannin extracts from acorns induced periacinar hepatic necrosis in mice. CONCLUSION: Wasting, diarrhoea and mortality in wild juvenile Australian king parrots were associated with Spironucleus-like protozoa in the intestine. Acorns were not considered to be the cause of the syndrome.

Animals↗
PubMed2000

Bumps on the managed care road: the search for an alternative model to reduce collisions between HMOs, physicians, and patients.

Managed care is experiencing political, litigious, and financial bumps on the road. There are various reasons for this bumpy ride: out-of-control costs, prescription drug expense, negative media reports, public revolt at denials of care or limited access to specialists, bad physician relations, patients' rights legislation, dropping health maintenance organization (HMO) stock prices, the ripple effect of the Harvard Pilgrim bankruptcy, and threat of massive litigation against HMOs. Two reasons not often mentioned, but explored in this article, are the orthodox managed care's flawed market model and lack of enough understanding of physician culture and emerging consumer trends to effectively address these two key constituencies.

Conflict, Psychological↗
PubMed1997

S-100 immunoreactivity in melanomas of two marsupials, a bird, and a reptile.

S-100 proteins are abundant in melanocytes of the skin; thus, S-100 immunoreactivity has been used as a diagnostic criterion for melanoma in humans and other placental mammals. We tested cutaneous melanomas of two marsupials, a bird, and a snake for S-100 immunoreactivity, using a polyclonal rabbit antibovine S-100 antibody. The tumor from a Tasmanian Pademelon (Thylogale billaridierii) was composed of large epithelioid cells, most of which had S-100-positive cytoplasm. In general, there were only scattered individual spindle-shaped S-100-positive cells or groups of cells in the primary mass from a Spotted-tailed Quoll (Dasyurus maculatus); S-100 staining was primarily nuclear. Cells comprising the melanomas of the Australian Cormorant (Phalacrocorax carbo) and the Death Adder (Acanthophis antarcticus) were S-100-negative, although peripheral nerve bundles in both were S-100-positive.

Animals↗
PubMed1997

Encephalomyocarditis virus infections in an Australian zoo.

Fatal encephalomyocarditis virus (EMCV) infections in a ring-tailed lemur (Lemur catta), a squirrel monkey (Saimiri sciureus), three mandrills (Mandrillus sphinx), a chimpanzee (Pan troglodytes), a pygmy hippopotamus (Choeropsis liberiensis), and two Goodfellows tree kangaroos (Dendrolagus goodfellowi) occurred at Taronga Zoo. This is the first description of EMCV in a zoological collection outside of the United States. Regardless of species, the most common clinical presentation was sudden death. The gross pathologic changes were diffuse or focal pallor of the myocardium with occasional marked pulmonary congestion. Necrotizing nonsuppurative myocarditis was consistently present. EMCV was isolated from only one of 54 feral rodents examined. No antibodies to EMCV were detected with a serum neutralization test in 79 stored sera from a wide variety of zoo mammals. Titers of 1:16, 1:16, and 1:4 were recorded for a spider monkey (Aeteles geoffroyi), a lion (Panthera leo), and an orangutan (Pongo pygmaeus), respectively. Of seven mandrills tested in 1988, six had measurable virus titers. Later testing indicated that these titers did not persist, and one mandrill with a titer > 1:128 in 1988 subsequently succumbed to EMCV infection in 1991.

Animals↗
PubMed1993

Genetic differences in susceptibility of chicken lines to infection with infectious bursal disease virus.

Mortality rates in 11 inbred and partially inbred chicken lines inoculated with a very virulent strain (CS89) of infectious bursal disease virus (IBDV) varied considerably, being highest (almost 80%) in a Brown Leghorn line (BrL). Bursa of Fabricius to body weight ratios were depressed in the survivors in each line, but no differences were observed between lines. However, histological examination of bursae from survivors showed that, although bursal damage occurred in every line, it was most severe in the two lines (BrL and White Leghorn W1) in which the highest mortality was recorded. Experiments with F1 matings between highly susceptible and highly resistant lines showed that resistance was partially dominant and that there were no maternal effects. Experiments using F2 and backcross chicks suggested the involvement of a single gene and indicated no involvement of the MHC. There was considerable variation between lines in IBDV-specific antibody, measured by ELISA, both in the vaccinated parent hens and in the amounts of inherited maternal antibody and its rate of decay in the progeny.

Aging↗