94 N.J. Fox et al.
immunity. Possum susceptibility has been dem-
onstrated in experimental infections, where
aerosol or intra-tracheal administration of
10–100 colony forming units (CFU) leads to
rapid disease progression and death in 8–10
weeks (Aldwell et al., 2003).
In infected possums, lesions are predomi-
nantly found in the lungs and peripheral superfi-
cial lymph nodes, with bacterial counts reaching
107 CFU/g of lung tissue (Nugent et al., 2015a).
Fulminating M. bovis in naturally infected pos-
sums is rapidly lethal, with possums showing
clinical signs of tuberculosis dying within an
average of 4.7 months (Ramsey and Cowan,
2003). In cachectic individuals in the terminal
stage, infections are often generalized, with
lesions in the liver, spleen, lungs or kidneys
(Jackson et al., 1995). At this stage, purulent
material can be discharged from suppurating
lesions in superficial lymph nodes (Gortazar
et al., 2015).
The mechanisms of infection are unclear,
and transmission experiments have shone little
light on the process (Corner et al., 2002). How-
ever, potential routes can be gleaned from lesion
distributions. In possums with tuberculosis,
lesions are common in the lungs (Jackson et al.,
1995) which, in non-ruminants, is indicative of
respiratory transmission. Evidence of respira-
tory transmission is further compounded by the
presence of M. bovis from tracheal washings and
the discharging fistula of superficial lymph
nodes, whereas bacterial isolation from urine
and faecal samples from infected possums is
rare. Lesions are also common in the peripheral
lymph nodes (e.g. the axillary and inguinal)
(Jackson et al., 1995), suggestive of percutane-
ous infection from scratches received during
fighting or mating. The presence of tuberculosis
lesions in possum mammary glands suggests
that pseudovertical transmission via milk may
occur (Jackson et al., 1995). It has been sug-
gested that initial infections in possums were
from spillover from wild deer, as the first out-
breaks in possums coincided with the beginning
of commercial deer hunting (circa 1960). It was
common practice to leave the heads and offal
from hunted deer in the field, leaving possums to
scavenge on potentially infected material
(Nugent, 2011).
7.1.2 BadgersBadgers (Meles meles) are considered the most
important wildlife host of M. bovis in the UK and
Ireland (Delahay et al., 2002; Phillips et al.,
2003), and infected animals have occasionally
been isolated from other countries (Bouvier
et al., 1962). Badgers are highly social animals
and at high densities form social groups that
defend distinct territories (Roper et al., 1986).
There is wide variation in estimates of M. bovis
prevalence in badgers, with infections showing
high spatial aggregation (Delahay et al., 2000;
Woodroffe et al., 2005). At the local population
level, there is no consistent correlation between
badger density and TB prevalence (Vicente et al.,
2007a; Delahay et al., 2013), although the
incidence of new cases does correlate with the
frequency of intergroup movements (Vicente
et al., 2007a).
The principal site of infection in badgers is
the lower respiratory tract, with a high fre-
quency of lung infections and high prevalence
of pulmonary lesions (Gallagher and Nelson,
1979; Gallagher and Clifton-Hadley, 2000;
Gavier-Widen et al., 2001; Jenkins et al., 2007a).
This suggests that inhalation of infectious aero-
sol particles and infection by the respiratory
route is the most likely route of transmission
(Gavier-Widen et al., 2001; Jenkins et al.,
2007a). In contrast, infection via the gastroin-
testinal tract is rare, possibly due to the highly
acidic conditions (Vandal et al., 2009). Bacilli
excreted in badger urine, sputum, faeces and
abscess pus are thought to contaminate the
environment (Gallagher et al., 1976; Gallagher
and Clifton-Hadley, 2000). Of the excreta, urine
from animals with infected kidneys has the
highest numbers of bacilli at 250 × 103 CFU/ml
urine (Gallagher and Clifton-Hadley, 2000).
As competent hosts, the majority of infec-
tions in badgers are latent, lesions are often
resolved, and even complete elimination of
M. bovis infection has been observed (Gallagher
et al., 1998). Consequently, badgers can sur-
vive infection for several years, excreting
bacteria while maintaining social interactions
( Cheeseman et al., 1989). Badgers of all ages are
susceptible; however, infection risk increases
with age (Jenkins et al., 2007a). Males have a