Badger cubs will be shot under plans to shift the controversial cull to early summer in 2015, the Guardian has learned.
The badger culls, aimed at curbing tuberculosis in cattle, have so far taken place in the autumn and have repeatedly missed their minimum kill targets. Cubs are easier to catch and shoot and are more numerous in early summer, making it more likely an earlier cull will hit its target.
But scientists have warned killing cubs rather than adults has less effect on cutting TB, while animal campaigners condemned the plan as “appallingly crude and desperate”.
The National Farmers Union (NFU), which speaks for the culling companies, said government licences permit culling to begin any time from June. The Department of Environment Food and Rural Affairs (Defra) said the timing of the culls was a decision for the culling companies.
Badger cubs are born underground in February and first emerge in April. While the cubs and their parents legally cannot be culled until the start of June, it is legal to shoot them under licence afterwards. The cullers intend to start in June or July 2015, according to Guardian sources.
However, leading badger expert Professor Rosie Woodroffe, at the Zoological Society of London, said: “They may well catch more badgers if they cull in June, because young cubs are naïve and easy to trap. But many of cubs die in their first year, especially in dry summers. So killing 100 badgers in June wouldn’t reduce the badger population as much as killing 100 badgers in November.
“Also, cubs are much less likely to have TB, so killing cubs would not have the same effect on reducing disease as killing adults.”
Well, this one isn't quite up there with introducing cane toads to Australia in terms of bonkers pest control ideas, but it is certainly up there with the daft ones.
ReplyDeleteThe object of the exercise here is to reduce bovine tuberculosis, the disease. Badgers are extremely good spreaders of this disease, because they have next to no immunological resistance to it (bTB needs an inflammatory response, like the anti-parasitic response, to be controlled; an anti-bacterial response merely churns out immunoglobulins, and bTB has this nasty trick of hiding from antibodies in a host...).
Vaccinating badgers against bTB has been shown by DEFRA not to prevent infection by wild-type bTB bacteria, so that isn't going to work. Reducing badger numbers does work, as the Hartland and Thornbury eradication experiments showed.
The way you eradicate a hard-to-find pest is you work out where it is easiest to find and when it is most vulnerable, and you hit it then. With rodent infestations, you mouse and rat-proof all buildings over summer, then bait like crazy during winter when they're not breeding as much.
With badgers, you wait until winter and gas the setts. As methyl bromide has rightly been banned, and hydrogen cyanide has welfare problems (you cannot guarantee hitting rapidly lethal levels everywhere in a sett), you fall back on thirty-odd years of Ministry of Agriculture research.
They had a solution twenty-odd years ago: carbon monoxide gas. This is lethal in quite low proportions, is odourless and tasteless and doesn't provoke a choking response, and is easy to synthesise on site. Thirty years ago the MoA weapon of choice was a petrol-fuelled Range Rover V8 running on full choke (diesel engines don't generate carbon monoxide; plenty of other vile nasties, but no CO), but obviously these days a cleaner, more controllable method would be used.
Finally, we have to think about the dynamics of how bTB works. bTB exists in a lot of different spoligotypes, which amount to races; genetically based, heritable and unchanging over time, and these let you see where each infection came from. Geographical spoligotype patterns have been very, very stable over time; it would appear that they don't drift at all, which is strange because the natural movement of badgers ought to give some drift, over a period of decades.
Recent research may hold an answer. The BCG vaccine strain of tuberculosis which is derived from bTB has been seen, under unusual circumstances, to make endospores. It only ever does so when the culture is old, food is running out and the culture is more or less dying on its feet, and that too is telling.
BCG can't do anything that wild-type bTB can't do, so it is likely that bTB can make spores as well. It too will only do so when its home is on the verge of dying; this equates to an animal dying or very recently dead of tuberculosis. Badgers, when they're feeling unwell, retreat underground to sleep it off and thus I reckon that the vast majority of bTB infected animals die underground.
What better place for bacterial endospores to survive and endure, than underground in 100% humidity and zero UV light? Perhaps it isn't so much the badger populations that are infected so much as their setts which are harbouring the disease as endospores in the soil?