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J W Galvin

Publications and source records attributed to J W Galvin.

11 recordsLinked to original sources
PubMed2005

A comparison of two ELISAs for the detection of antibodies to bovine leucosis virus in bulk-milk.

OBJECTIVE: To estimate the sensitivity, specificity and detection limits for two bulk-milk enzyme-linked immunosorbent assays, the Svanovir BLV-gp51-Ab and the Lactelisa BLV Ab Bi indirect tank 250, for the detection of antibody to bovine leucosis virus in milk. PROCEDURE: Milk samples from 27 cows known to have enzootic bovine leucosis (EBL) were serially diluted with milk from a herd known to be free from the disease. The dilution at which antibodies could no longer be detected by each test was determined. A total of 1959 bulk-milk samples submitted to a laboratory for the Victorian (EBL) eradication program were tested with both the Svanovir and the Lactelisa assays. A Bayesian approach was used to calculate maximum-likelihood estimates of test sensitivity and specificity. An additional 660 bulk-milk samples were tested with both the Svanovir and the Lactelisa assays. Herds that had positive results on either or both of the assays were subjected to blood or milk testing of individual cattle. RESULTS: The dilution of milk at which the Svanovir assay failed to detect enzootic bovine leucosis antibody in half of the samples was 1 in 40, whereas the comparable value for the Lactelisa was 1 in 200. Computer modeling of the operating characteristics of the Svanovir assay indicated that the sensitivity of that assay would be considerably lower than that for the Lactelisa, and the specificity was estimated to be higher. Evaluation of the assays using 660 bulk-milk samples showed that the Lactelisa assay detected four infected herds that were not detected by the Svanovir test. No false positive results were recorded for either assay. CONCLUSION: Use of the Lactelisa assay in the Victorian EBL eradication program will enhance disease detection and eradication, but may also result in an increased frequency of false positive bulk-milk test results.

Animals↗
PubMed2005

Killing of animals for disease control purposes.

In emergency disease outbreaks, large numbers of animals may need to be killed for control, containment and/or eradication purposes. Strategies for disease control will usually involve complete depopulation of herds/flocks, and may extend to depopulation across designated areas. Live animals present the major risk of spreading infectious agents so their slaughter should be completed as quickly as possible, with minimal pain and distress to the animals. The method chosen for killing of animals must be humane, efficient and safe for people and the environment. The tasks should be conducted under the supervision of an official veterinarian, supported by a sufficient number of adequately trained and competent personnel. It is essential to ensure all animals are dead, as demonstrated by the cessation of cardiac and respiratory movements. This paper discusses methods by which animals may be killed for disease control purposes.

Animals↗
PubMed2004

Effect of a test and control program for Johne's disease in Victorian beef herds 1992-2002.

OBJECTIVE: To report on progress in Johne's disease (JD) control in infected beef herds participating in the Victorian Johne's disease test and control program (TCP). PROCEDURE: Clinical histories and JD testing data recorded by the Department of Primary Industries were analysed for 18 beef herds participating in the TCP. The herds were required to conduct annual whole herd tests with an absorbed ELISA, cull reactors and control the grazing of young cattle to minimise infection. RESULTS: Testing of over 11,000 animals identified 68 reactors giving an average prevalence of reactors at the first whole-herd test round (T1) of 0.77%. There had been 20 clinical cases detected in the 7 years before the TCP started and two cases detected in the 10 years after TCP started. Most reactors and all clinical cases were born before the TCP started. Of 34 reactors necropsied, 25 (74%) were confirmed to have JD by histology or culture of tissues. The modal age of reactors and clinical cases was 5 and 6 years respectively. Six herds completed the program by achieving three successive negative whole herd tests, four herds dropped out and eight continued to test. There were 18 reactors detected at T1 and 33 reactors that were negative at T1 but detected at subsequent tests. CONCLUSION: The TCP was associated with a marked decline in clinical cases. The similar age distributions of clinical cases and reactors probably meant that testing detected animals for which clinical disease was imminent. Whether the measures used in the TCP were adequate to control the disease in beef herds could not be determined because of the long incubation period of the disease. The relatively high proportion of the reactors investigated that were confirmed as infected provided confidence that the test was continuing to operate at a high specificity. If all unconfirmed reactors were presumed to be uninfected, the minimum specificity of the ELISA was 99.83%. The sensitivity of the ELISA appeared to be very low because of the large number of reactors that were negative at T1 but positive at later tests.

Animals↗
PubMed2004

Effect of a test and control program for bovine Johne's disease in Victorian dairy herds 1992 - 2002.

OBJECTIVE: To report on progress in Johne's disease (JD) control in infected dairy herds participating in the Victorian Johne's disease Test and Control Program (TCP). PROCEDURE: Clinical histories and JD testing data recorded by the Department of Natural Resources and Environment (now called Department of Primary Industries) were analysed for 542 dairy herds participating in the TCP. The herds were required to conduct annual herd tests of cattle 2 years old and older with an enzyme linked immunosorbent assay (ELISA), cull the reactors and manage the younger cattle to minimise infection. RESULTS: Testing of over 680,000 animals identified over 10,000 reactors giving an average prevalence of reactors at the first whole-herd test (T1) of 1.78%. There was a relatively rapid increase in the incidence of clinical disease before the TCP started and then it markedly declined. There was a slow and interrupted decline in reactor prevalence, with a marked peak occurring at the fourth herd test (T4). The average age of reactors and clinical cases was 5.7 and 5.9 years, respectively. Of the reactors and clinical cases detected during the TCP, 87% and 95% respectively, were born before the TCP started. Thirty herds completed the program by achieving three successive negative whole herd tests and 91 herds dropped out because of inability to comply with the agreed requirements of the program. There were no home-bred reactors born after the start of the program in 253 (47%) herds and of the 522 herds that were tested more than once, there were 319 (61%) herds in which no home-bred reactors were detected after the first year of testing. The number of ELISA positive animals detected at T1 appeared to be only about 26% of the animals from that round that subsequently became positive or developed clinical disease at later test rounds. CONCLUSION: The TCP caused a marked decline in the number of clinical cases, probably because animals in which clinical disease was imminent were detected by testing and removed. A reduction in prevalence of reactors occurred only when most herd members were born after the TCP started. The sensitivity of the ELISA appears to be low based on the large number of reactors that were negative at T1 but were positive at later tests. Low sensitivity of diagnostic tests and the long incubation period of the disease limits meaningful analysis of the program until it has continued for some years. Measures adopted in the TCP have not broken the cycle of infection in many participating herds. It is unsure if this was because of poor compliance with control recommendations or a poor understanding of methods of transmission by scientists. Eradication is not feasible in the short-term.

Animals↗
PubMed1999

Anthrax explodes in an Australian summer.

Anthrax occurred on 83 properties in an area of north central Victoria between 26 January and 26 March in the summer of 1997. Anthrax had not been recorded in the outbreak area since records were initiated in 1914, although anthrax did occur in the general area in the 1880s to 1890s. Standard Australian control measures were applied to the properties, including quarantine, tracing movements of animals on and off affected properties, secure disposal of carcases by burning, enhanced surveillance of stock generally in the area and the use of local disaster control procedures including an alert of health authorities. As affected property numbers began to increase dramatically from 8 February, it was decided to use blanket area vaccination to control the disease. By 26 February, the epidemic curve had returned to the base line and a buffer vaccination zone of 457 farms holding 78,649 cattle was formed by early March 1997. Between 26 January and 26 March when the outbreak was declared over, 202 cattle and 4 sheep were confirmed to have died of anthrax. Between 27 March and early November a further 26 cattle were confirmed as dying due to anthrax and 14 of these had not had previous vaccination, including four young calves and one horse. One new property within the vaccination buffer zone had an anthrax case in a cow in early November 1997. By mid-November 1997, all previously infected and all neighbouring properties within 1 km were compulsorily re-vaccinated, as were all calves when two months of age and all introduced cattle. In 1998, only two confirmed cases of anthrax were diagnosed; both were vaccinated calves on farms which had had multiple cases during the outbreak. The public reaction and attention fueled by unprecedented media attention led to intense international scrutiny from countries where anthrax is a particular zoonotic problem. Very strong representations had to be made about the safety of livestock and livestock products that came from Victoria. This event has demonstrated that there is a need to review OIE and other requirements and recommendations covering anthrax where strict restrictions are placed on livestock and livestock products to protect livestock and human populations against anthrax infection.

Animals↗
PubMed1999

Experiences with vaccination and epidemiological investigations on an anthrax outbreak in Australia in 1997.

Between January and February 1997, there was a severe outbreak of anthrax on 83 properties in north-central Victoria, Australia. Vaccination was used as a major tool to control the outbreak by establishing a vaccination buffer zone 30 km by 20 km. In all, 78, 649 cattle in 457 herds were vaccinated in a three week program. In the face of the outbreak, there was a delay before vaccination was able to stop deaths. In the 10 days following vaccination 144 cases of confirmed anthrax occurred and 38 cases occurred more than 10 days after vaccination. When all cattle on at-risk properties were revaccinated in October and early November 1997, there were only two confirmed cases of anthrax in vaccinated seven and nine month old calves in the following anthrax season. Investigations into the epidemiology of the outbreak were unable to establish a single major association for the spread of the disease by flies, biting insects, carrion scavengers, wind, manufactured feed, milk factory tanker routes, veterinary visits, animal treatments, movements of personnel between farms or burning of carcases. The weather conditions in the outbreak area were part of a long dry spell with periods of high daily and night temperatures, continuing high humidity over the period and higher than normal soil temperatures. It is possible that extensive earth works in the district involving irrigated pasture renovation and water channel and drainage renovation could have disturbed old anthrax graves. It is postulated that these works released spores that were dispersed in the preceding wet winter across poorly drained areas that formed the axis for the outbreak. The earth moving renovations establishing irrigation in the area were conducted in the late 1890s, and before the occurrence of anthrax outbreaks were recorded. The axis of the outbreak was the major stock route for cattle and sheep moving from southern Victoria to northern Victoria and southern New South Wales, and undoubtedly there would have been extensive anthrax outbreaks before vaccine became available in the 1890s. In respect of other outbreaks, the events in Victoria most resembled outbreaks of anthrax recorded in the United States of America in the 1950s, 1960s and 1970s.

Animals↗
PubMed1993

Chlamydiosis in workers at a duck farm and processing plant.

An outbreak of chlamydiosis was investigated in workers at a duck farm and processing plant during winter 1989. Chlamydia psittaci was isolated from ducks, but there was little evidence of clinical chlamydiosis in the ducks. Serological tests showed that 76% of workers had been exposed to infection, 12% recently, 16% had not been exposed and 8% had inconclusive test results. There was a strong association (P < 0.05) between years of employment and exposure to infection. Infection appeared to be contracted during the first year of employment. Measures were implemented to reduce shed contamination and control rodents and wild birds. At the same time, ducks were medicated, the processing plant was modified, work practices were altered and workers were advised about chlamydiosis to reduce the risk of human infection.

Adult↗
PubMed1992

Management of land and livestock contaminated with polychlorinated biphenyls.

Investigations were conducted on several small neighbouring beef cattle and sheep farms that were found to be contaminated with polychlorinated biphenyls (PCBs). The residues detected contained about 62% w/w chlorine and soil concentrations ranged from 0.35 to 1.9 mg/kg. Beef cattle and sheep grazing the contaminated land had PCB concentrations in their fat of 0.3 to 1.7 mg/kg and 0.19 to 0.45 mg/kg, respectively. The concentration of PCBs in the caudal fat of cattle was 0.3 to 2 times the concentration of PCBs in the land they were grazing and was positively related to stocking rates. PCBs were present in milk fat from cattle at about the same concentration as in caudal fat, and lactation appeared to contribute to decontamination. Wool grease from sheep contained about 1 to 2 times the concentration of PCBs in subcutaneous fat. Calves of contaminated cows also became contaminated. The half-life for decontamination of PCBs in a group of 8 young female beef cattle was calculated at 13 months. PCBs were detected in pasture samples at concentrations ranging from less than 0.01 mg/kg to 0.12 mg/kg. However, PCBs were not detected in any sample of hay cut from these paddocks. In 4 sheep fed a sole ration of this hay, traces of PCBs were detected in their fat following 89 days of feeding. Grazing livestock for meat production on land contaminated with PCBs is not recommended because livestock readily acquire residues, and PCBs persist in soil and livestock for long periods. Grazing sheep for wool production on land contaminated with PCBs may be an option.

Adipose Tissue↗
PubMed1985

An outbreak of botulism in wild waterbirds in southern Australia.

An outbreak of Type C botulism in waterbirds was investigated at Lake Lalbert in northwestern Victoria, Australia. Total losses were estimated at 1,500 birds, with 80% of affected birds being grey teal (Anas gibberifrons). The outbreak was associated with a falling water level, and extensive decomposition of plant material.

Animals↗