MicrobiologyBytes

I’m trying to persuade a student to do my final year project next year on badger culling and bovine tuberculosis:

Bovine tuberculosis (bTB) remains an important public health concern worldwide as a result of deficiencies in preventing and/or controlling measures targeting the spread of its causative agent Mycobacterium bovis. While the risk posed by M. bovis to human health is low in most developed countries, the main causes of concern related to M. bovis in industrialized countries are epizootics in domesticated and wild mammal populations. Infection with M. bovis remains a significant livestock zoonosis in the European Union where some member states experience a reemergence of the disease despite significant historical efforts to implement eradication plans. In Great Britain, the disease was eliminated from most cattle herds by 1960, with the exception of infection hotspots in southwest England, after the implementation of a herd testing and slaughter policy. However, efforts to completely eradicate bTB in Great Britain have been hampered by the maintenance of M. bovis in wildlife host populations, acting as reservoirs of infection, in particular badgers (Meles meles). Since 1979, incidence in British cattle has increased and the infection has become more geographically widespread. Over 7 million cattle were tested for bovine bTB in 2009 and one in ten herds experienced bTB-related movement restrictions during the year as a result of at least one member of the herd failing the tuberculin skin test or showing lesions consistent with bTB during the slaughterhouse inspection – an event known as a “herd breakdown”.

Local Cattle and Badger Populations Affect the Risk of Confirmed Tuberculosis in British Cattle Herds. 2011 PLoS ONE 6(3): e18058. doi:10.1371/journal.pone.0018058
Background: The control of bovine tuberculosis (bTB) remains a priority on the public health agenda in Great Britain, after launching in 1998 the Randomised Badger Culling Trial (RBCT) to evaluate the effectiveness of badger (Meles meles) culling as a control strategy. Our study complements previous analyses of the RBCT data (focusing on treatment effects) by presenting analyses of herd-level risks factors associated with the probability of a confirmed bTB breakdown in herds within each treatment: repeated widespread proactive culling, localized reactive culling and no culling (survey-only).
Methodology/Principal Findings: New cases of bTB breakdowns were monitored inside the RBCT areas from the end of the first proactive badger cull to one year after the last proactive cull. The risk of a herd bTB breakdown was modeled using logistic regression and proportional hazard models adjusting for local farm-level risk factors. Inside survey-only and reactive areas, increased numbers of active badger setts and cattle herds within 1500 m of a farm were associated with an increased bTB risk. Inside proactive areas, the number of M. bovis positive badgers initially culled within 1500 m of a farm was the strongest predictor of the risk of a confirmed bTB breakdown.
Conclusions/Significance: The use of herd-based models provide insights into how local cattle and badger populations affect the bTB breakdown risks of individual cattle herds in the absence of and in the presence of badger culling. These measures of local bTB risks could be integrated into a risk-based herd testing programme to improve the targeting of interventions aimed at reducing the risks of bTB transmission.

Related:

• Public health and bovine tuberculosis
• Culling badgers a low priority for curbing cattle tuberculosis
• Irish badger cull ‘futile’ in controlling bovine tuberculosis

Prions are transmissible, proteinaceous agents that cause fatal neurodegenerative diseases. In deer elk moose prions cause chronic wasting disease (CWD). The incidence of CWD can be remarkably high both in captive and wild herds and epidemiological data suggest that efficient horizontal transmission drives epidemic dynamics. Although deer can be infected orally and seem to be able to contract CWD from contaminated environments, precisely how and when CWD prions are shed into the environment have not been described. Previous studies have identified CWD prions in saliva, blood, urine, antler velvet, and muscle, lymphoid and other tissues of symptomatic cervids with late-stage disease. These sources of CWD prions may contribute to the spread of CWD, but none explains natural CWD transmission both within and between species in the deer family. To fit observed patterns, a natural CWD transmission mechanism must be effected within biologically realistic limits of the carrier medium, cannot require cannibalism and should be indirect to explain both environmental persistence and spread among multiple host species. Because empirical data and modelling suggested faecal excretion of prions throughout much of the disease course as potentially important to CWD transmission, researchers investigated whether prions are shed in faeces from mule deer during the course of CWD infection.

Asymptomatic deer excrete infectious prions in faeces. 2009 Nature 461: 529-532 doi:10.1038/nature08289
Infectious prion diseases – scrapie of sheep and chronic wasting disease (CWD) of several species in the deer family – are transmitted naturally within affected host populations. Although several possible sources of contagion have been identified in excretions and secretions from symptomatic animals, the biological importance of these sources in sustaining epidemics remains unclear. Here we show that asymptomatic CWD-infected mule deer (Odocoileus hemionus) excrete CWD prions in their faeces long before they develop clinical signs of prion disease. Intracerebral inoculation of irradiated deer faeces into transgenic mice overexpressing cervid prion protein (PrP) revealed infectivity in 14 of 15 faecal samples collected from five deer at 7–11 months before the onset of neurological disease. Although prion concentrations in deer faeces were considerably lower than in brain tissue from the same deer collected at the end of the disease, the estimated total infectious dose excreted in faeces by an infected deer over the disease course may approximate the total contained in a brain. Prolonged faecal prion excretion by infected deer provides a plausible natural mechanism that might explain the high incidence and efficient horizontal transmission of CWD within deer herds, as well as prion transmission among other susceptible cervids.

Why should we care?
Apart from the impact on wildlife, vCJD is a prion infection transmitted from infected cows to humans. People eat deer. Although there is no evidence that the CWN prion causes diseae in humans, this is definitely one to keep an eye on.

Related:

• A General Model of Prion Strains and Their Pathogenicity
• Prions, Proteasomes, and Mad Cows
• Oral transmission of prions is enhanced by binding to soil
• Prions and Cheetah Conservation