Dr John Gallagher, a veterinary pathologist since 1972
THE NATURE OF TB IN BADGERS
1.Tuberculosis has a different manifestation in most species . In the badger it is fundamentally different from TB in cattle essentially due to the lack of development of a hypersensitivity response which is a prime feature of infection in cattle. Thus small numbers of organisms infecting cattle produce a vigorous cellular response which results in extensive cell death and the development of large cold abscesses in the affected tissues usually the lung and
respiratory lymph nodes . This is in fact the host immune reaction to TB. Whilst causing disease and disruption to the affected organs the changes inside these abscesses strongly inhibit the TB bacteria and kill many of them.
The badger does not show such a vigorous destructive reaction but rather a slowly progressive proliferative reaction
which eventually results in cell death as numbers of bacteria increase markedly. TB lesions are thus relatively much
smaller but contain relatively vastly more bacteria than those of cattle. TB bacteria do not produce toxins but rather cause lesions as a result of their highly antigenic cell walls to which different hosts may respond with greater or lesser
aggression.
PROGRESSION OF INFECTION
2. Once a badger develops disease all the members of that social group are likely to become infected due to the confined living space in their underground tunnel systems, their highly gregarious nature and constant mutual grooming. But that seed of infection (the primary focus ) will usually only progress to produce disease and eventually death in a minority of cases. Latency is a feature of TB in many species and this is so in badgers and cattle. The bulk of infections in badgers, usually 70% or more will become latent or dormant. A small number of badgers may resolve the infection completely and self cure. But the latent infections remain fully viable and may breakdown under stress which may be of nutritional origin, intercurrent disease, senile deterioration or social disturbance and disruption. Some badgers may develop fulminating disease (Gallagher et al 1998).
Badgers with terminal generalised tuberculosis can excrete vast numbers of bacteria particularly when the kidneys are
infected. Counts of several million bacteria in a full urination have been recorded (Gallagher and Clifton-Hadley, 2000).
When infection is acquired by a bite wound from the contaminated mouth of another badger, the bacteria are Inoculated either deeply subcutaneously or intramuscularly and rapid generalisation of infection usually occurs, causing progression to severe and often fatal tuberculosis which may develop in a matter of several months (Gallagher and
Nelson, 1979). Respiratory origin infections have a longer duration and cases in an endemically infected population (Woodchester) have been monitored showing intermittent excretion of infection for a year, with the longest recorded case excreting for almost three years before death.
The above ground mortality due to TB is estimated as about 2% of the population per annum. Thus in the South West
alone with its now extensive endemically infected areas the annual deaths due to TB will be of the order of at least 1000 to 2000.
Tuberculosis has an unfettered progress in the badger population and the cycle of infection and disease in the badger has long been known to be self sustaining (Zuckerman 1980). Over time the badger has become well adapted as a primary reservoir host of bovine TB infection.
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