The ovine strain of M. ptb used in this study was less virulent for red deer than the bovine strain. The correlation between dose of the bovine strain and the severity of lesions suggests that clinical Johne's disease in yearling red deer likely results from high oral challenge with a bovine strain whilst they are young. The minimum oral infective dose may be close to 10(3) cfu for this bovine strain.
Tuberculosis (Tb) caused by Mycobacterium bovis is a worldwide threat to livestock and humans. One control strategy is to breed livestock that are more resistant to Mycobacterium bovis. In a 3-year heritability study 6 farmed red deer stags were selected from 39 on the basis of their differing responses to experimental challenge via the tonsillar sac with approximately 500 CFU of M. bovis. Two stags remained uninfected, two were moderately affected, and two developed serious spreading Tb. Seventy offspring, bred from these six stags by artificial insemination using stored semen, were similarly challenged with M. bovis. The offspring showed patterns of response to M. bovis challenge similar to those of their sires, providing evidence for a strong genetic basis to resistance to Tb, with an estimated heritability of 0.48 (standard error, 0.096; P < 0.01). This is the first time the heritability of Tb resistance in domestic livestock has been measured. The breeding of selection lines of resistant and susceptible deer will provide an ideal model to study the mechanisms of Tb resistance in a ruminant and could provide an additional strategy for reducing the number and severity of outbreaks of Tb in farmed deer herds. Laboratory studies to identify genetic and immunological markers for resistance to Tb are under way. Preliminary studies showed no associations between NRAMP or DRB genes and resistance to Tb in deer. Patterns of immune responses seen in resistant animals suggest that both innate and acquired pathways of immunity are necessary to produce the resistant phenotype.Tuberculosis (Tb) is one of the most widespread diseases of mankind and animals. Although the majority of cases of human Tb are caused by Mycobacterium tuberculosis, a small proportion are caused by Mycobacterium bovis carried by cattle and other domestic animals (25). In order to reduce this zoonotic risk, most developed countries have attempted to eradicate bovine Tb from their domestic animals. The problem is compounded by the establishment of Tb in wildlife reservoirs such as badgers in the United Kingdom (31) and Ireland (8,23), buffalo and antelope in South Africa (25), and bison and deer in North America (25). In New Zealand, traditional "testand-slaughter" control methods (24) and the killing of wildlife vectors, such as opossums (Trichosurus vulpecula) and ferrets (Mustela furo), have nearly halved the prevalence of Tb on farms in the last 5 years. The percentage of infected herds was 1.5% of the 60,000 cattle herds and 2.3% of the 5,200 deer herds recorded at the end of June 1998 (2). However, to reach the internationally accepted level of 0.2% herd infection rate, additional strategies are needed. One strategy for reducing the incidence of Tb in domestic livestock, which has not been used previously, is to select for increased genetic resistance.Red deer have been farmed in New Zealand for more than 25 years, and they currently number over 1.7 million on approximately 5,200 farms. At the end of June 1998 there were 118 known infected her...
Vaccination of farmed deer with an oil-adjuvanted Johne's vaccine has the potential to cause significant interference with routine tuberculin skin testing. The cross-reactivity should decline with time and the CCT should be able to clear MCT-positives, but there is a risk of false-positives to the blood test for tuberculosis (BTB), due to high persistent levels of antibody. The CCT could be used as a primary skin test in vaccinated deer on some farms. The Aqueous Ptb caused fewer problems with skin testing and produced significantly less bovine antibody than the Oil-adjuvant Ptb, but stimulated persistent cell-mediated immune responses that may provide some protection against Johne's disease.
The experimental challenge with M. ptb produced subclinical Johne's disease in the majority of deer, but did not cause any clinical disease. The number and severity of gross and microscopic lesions was significantly reduced in the COM compared with Control and EXP groups; vaccination of the EXP group did not appear to give significant protection. Deer vaccinated with the commercial vaccine are likely to give a false-positive reaction to the MCT but should have an avian reaction to the CCT, if it is carried out >12 months after vaccination. Most of the deer vaccinated with the commercial vaccine produced significant levels of antibodies against both M. ptb and M. bovis, which interfered with ancillary Tb tests. If this vaccine or similar oil-based vaccines are used on deer farms in the future, it may be advisable to only vaccinate animals destined for slaughter, that would not need to be Tb-tested, but would be 'works-monitored' for evidence of Tb instead.
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