Animal, page 1 of 11 © The Animal Consortium 2019

doi:10.1017/S1751731118003403
animal

Prevalence of an inflammation and necrosis syndrome in suckling

piglets
G. Reiner1†, M. Lechner2, A. Eisenack3, K. Kallenbach4, K. Rau4, S. Müller4 and
J. Fink-Gremmels5
1
Department of Veterinary Clinical Sciences, University of Giessen, Frankfurter Strasse 112, 35392 Giessen, Germany; 2UEG Hohenlohe-Franken, Kraussenklinge 1,
97996 Adolzhausen-Niederstetten, Germany; 3Veterinary Practitioner, Antoniusstr 38, 53909 Zülpich, Germany; 4Thuringian State Institute of Agriculture,
Naumburger Str. 98, 07743 Jena, Germany; 5Faculty of Veterinary Medicine, Utrecht University, IRAS, Yalelaan 104, 3584 CM Utrecht, The Netherlands

(Received 4 April 2018; Accepted 19 November 2018)

The current study describes the results obtained from clinical examination of over 4700 suckling piglets from 19 individual herds in
Germany. In this cohort the prevalence of inflammation and necrosis in the tails, ears, claw coronary bands, heels and teats was
determined using a pre-defined scoring system. Results show that already in the 1st days of life, piglets were affected by
inflammation and necrosis of the heels (80%), claw coronary bands (50%) and tail base (20%). The praevalences of these
alterations in piglets were influenced by genetics ( P < 0.001) and age, decreasing gradually in the 2nd week of life ( P < 0.001).
Moreover, a correlation between tail length after tail docking and the prevalence of tail necrosis ( P ⩽ 0.04) was found. Tail and ear
biting as a behavioural trait was not detected during this study. The early onset, appearance and multiple locations of clinical signs
of inflammation and the positive correlation with the genetic background of the piglets may suggest an impairment of the innate
immune system by infectious and non-infectious agents. This is in contrast to previously described behavioural abnormalities seen
in fattening pigs. Considering the obvious reduction of animal welfare due to the described lesions, there is a need to create
awareness among pig farmers and to understand the multifactorial causality involved in this inflammation and necrosis syndrome
in piglets.

Keywords: pigs, tail necrosis, genetics, animal welfare

Implications climate control, nutrition at different stages of life and the

We here present a clinical scoring system for piglets that can
be used to identify litters or herds with a high prevalence of
clinical signs of inflammation and necrotic lesions, at the tail,
ears, claws and nipples in this age group. The prevalence of
inflammatory lesions is associated with the animals’ genetic
background and with the practice of tail docking, being
higher in piglets with undocked tails. These lesions, collec-
tively described as swine inflammatory and necrosis syn-
drome (SINS) are impairing animal welfare, but clearly differ
from earlier described clinical conditions of fattening pigs.
Introduction
Ensuring animal welfare is one of the major challenges in
modern pig farming. Animal welfare is influenced by multiple
factors such as animal genetics, farm management, stocking
density and animal handling, housing facilities including
†
E-mail: gerald.reiner@vetmed.uni-giessen.de
stimulation of natural (species-specific) behavioural traits, for
example, by the application of roughage and/or pen enrich-
ment materials (e.g. see, Van de Weerd and Day, 2009; Nan-
noni et al., 2016; Nasirahmadi et al., 2017). In fattening pigs,
welfare scoring schemes comprise various behavioural para-
meters such as alertness, general behaviour (restlessness and
aggressiveness) and the use of enrichment (percentage of pigs
actively using enrichment materials) (e.g. see, Studnitz et al.,
2007; Casal-Plana et al., 2017; Winfield et al., 2017; Lingling
et al., 2018). Impairment of animal welfare can also be asso-
ciated with suboptimal health conditions such as an increased
prevalence of lameness, loss of tail integrity and tail lesions, or
any other signs of inflammation, and the number of animals
requiring treatment/hospitalization (European Food Safety
Authority (EFSA) 2012 and 2014).
Tail lesions induced by tail biting are of special interest,
not only due to their severe impact on animal welfare, but
also in the light of the demands to ban tail docking in the EU
(EU directive 2008/120/EC). Field observations and scientific
studies have shown that discontinuing tail docking under

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Reiner, Lechner, Eisenack, Kallenbach, Rau, Müller, Fink-Gremmels
current practical conditions can increase the prevalence of
tail biting (Valros et al., 2004; Lahrmann et al., 2017). While
various factors may induce tail biting (EFSA, 2007; D’ Eath
et al., 2014), earlier studies focussed on tail-biting as a
behavioural disorder attributable to the barren environment
and housing conditions. However, even under extensive
outdoor conditions as they are the common practice in
Switzerland, a prevalence of tail biting between 14% and
20% was recorded in 2004 (Walker and Bilkei, 2006). This
suggests that three causalities have to be distinguished: tail
biting as a behavioural disorder (also denoted primary biting;
Taylor et al., 2010), and secondary biting of pre-damaged
tails, where the victim tolerates interactions with pen mates,
due to a primary inflammatory process resulting in ischemic
tail lesions. Moreover, tail necrosis without biting can be
observed. Currently, the cause of such secondary tail biting is
controversially discussed (EFSA, 2007; D’ Eath et al., 2014),
but the implementation of the non-docking policy requires
further understanding of the reasons for tail lesions that are
observed in modern pig production.
In addition to tail lesions, inflammation and necrosis of the
ears of pigs kept in production systems have been described
(Pringle et al., 2009; Pejsak et al., 2011; Papatsiros, 2012;
Weissenbacher-Lang et al., 2012; Park et al., 2013). For
example, Pejsak et al. (2011) described an ear necrosis syn-
drome in weaners and fatteners and discussed the possible
association with (sub-) clinical infections with Mycoplasma suis
as well as Staphylococcus hyicus and Streptococcus suis. Park
et al. (2013) associated ear necrosis with environmental factors
and infections with Staphylococcus aureus and Staphylococcus
hyicus. In these previous investigations it remained, however,
unclear, whether the pathogens were causative or secondary
invaders. Papatsiros (2012) associated ear necrosis (porcine
necrotic ear syndrome) in weaners with Porcine Cirocvirus
Type 2 (PCV-2) infections and recommended to intensify
vaccination control. Earlier, Pringle et al. (2009) associated
necrotic ear lesions with Treponema socranskii. In contrast,
Weissenbacher-Lang et al. (2012) described a comparable
syndrome, denoted PENS (porcine ear necrosis syndrome) in 5
to 10-week-old pigs. The authors investigated the prevalence
of infectious agents in the herd, such as Streptococci, Sta-
phylococci and Mycoplasmata, but could not detect any of
these agents in the affected animals. The authors proposed
that other (non-infectious) causes, such as mycotoxin expo-
sure or stress factors, should to be considered as primary
cause of PENS. Indeed, recent investigations showed that
exposure of pregnant sows to the mycotoxin DON (deoxy-
nivalenon) resulted in typical necrotic tail lesions even in
neonatal piglets (Van Limbergen et al., 2017).
The current study was designed to achieve a first indication
of the prevalence of such inflammatory reactions in piglets
from conventional pig farms. The decision to focus on young
piglets was made in consideration of the fact that some
common stressors such as high stocking density, crowding
and poor climate control, pen construction (flooring)
probably are less prominent risk factors at this early age. For
the assessment of clinically visible alterations, such as
2
inflammatory reactions and necrotic lesions on the tails, ears,
coronary bands, heels and teats of suckling piglets a scoring
system was developed and applied in a cohort consisting of
more than 4700 piglets from 19 individual herds, which had
been randomly selected in one geographic region.
Material and methods
Ethical statement
This study was supported by Thuringian piglet producers in
Germany and conducted in agreement with the responsible
authorities (Landesamt für Verbraucherschutz, Thuringia,
Germany; AZ: 22.2684-04-07-001/16).
Herds and animals
Between October 2015 and May 2016, data from 4725 pig-
lets from 382 litters in 19 herds were collected. These num-
bers were not obtained by sample size calculations. Rather,
they resulted from herd sizes of the farms that were willing to
participate in the investigation. The herds were randomly
selected, but all had reported a high prevalence of tail
lesions, since they had started to phase-out tail docking from
the beginning of 2015. Litters (12.4 ± 1.7 piglets (mean
± SD)) were monitored at an age of 5.5 ± 2.7 days to allow a
statement on the early suckling piglet phase. The herds were
visited at a time when most litters were about 4 to 7 days
old. Younger and older litters, if any, were also examined.
Each litter was monitored only once. Each herd had one of
four different genetic lines of sows (G1, 6 herds, 123 litters;
G2, 5 herds, 99 litters; G3, 6 herds, 120 litters; G4, 2 herds,
40 litters). These were typical production lines of various
breeding companies (not further specified). The herds used
Pietrain (13 herds, 263 litters) or Duroc boars (6 herds, 119
litters) to produce hybrid fatteners. Piglets were traditionally
tail-docked by cutting-off approximately one-half (13 herds,
224 litters with 2807 piglets) or one-third (tip-docking: 6
herds, 148 litters with 1824 piglets). The selection was made
by the farmer. The selected litters per herd were kept in the
same unit in direct proximity to each other to avoid a housing
bias. At the time of the experiment, four out of the 19 herds
additionally produced piglets without tail docking (n = 94).
These herds simultaneously used litters tail-docked by one-
half, tail-docked by one-third and litters without tail-docking.
Because of this relatively small number of litters with piglets
without tail docking, these animals were excluded from all
analyses except the direct comparison between the three
degrees of docking.
Housing and husbandry
Herds had on average 1000 sows, producing with 1- or 3-
week rhythms. Sows were vaccinated against porcine
parvo virus and erysipelothrix in each herd. Most herds
vaccinated piglets also against Mycoplasma hyopneumo-
niae and Porcine circovirus type 2. Sows and litters were
kept in farrowing pens (2.4 × 2.0 m) with farrowing crates
(2.0 × 0.7 m) during the entire lactation period. Sows were

stabled about 1 week before farrowing. They did not receive
any nesting material. The lactation period varied between
herds from 21 to 28 days. The temperature in the farrowing
rooms was set at 18°C to 22°C, with supplemental heat pads
and heat lamps provided for the younger piglets (for up to
10 days). The pens were provided with upper-floor ventila-
tion and slatted (polyvinylchloride) floors with only minor
differences due to different suppliers, without straw or any
other rooting material. The lactation diet (dry or liquid) was
formulated to meet or exceed standard requirements for all
nutrients, and in most cases obtained from commercial feed
mills. Sows were not additionally supplemented with
roughage. Water was supplied by so-called mother–child
troughs or by individual troughs for sows and piglets. Litters
were cross-fostered to 13/14 piglets no later than 48 h after
birth. Tail docking, teeth grinding and surgical castration of
male piglets after the application of an analgesic (0.2 ml
meloxicam i.m.; Metacam™, Boehringer, Ingelheim) was
performed at an age of 2 to 3 days. Iron (Fe3 + -hydroxide-
dextran complex) was routinely administered to all piglets
according to the specific product information.
Clinical scores
All litters were scored by a standardized clinical scoring
system for the number and percentage of piglets that
showed signs of inflammation and necrosis of the tail,
inflammation of the ear base, inflammation of the heels,
inflammation of the coronary band, inflammation/necrosis
of the teats, inflammation of the umbilicus, swelling of
the vulva and facial oedema and/or injuries. The scoring
systems for the piglets was binary (0 = normal;
1 = affected). Examples of typical lesions are shown in
Figures 1 to 8. Grades of clinical signs were not further
differentiated. All examinations in any of the herds were
conducted by the same two persons after a thorough
introduction and training programme. All piglets were
validated by both persons together; therefore there were
no inter observer effects. The observers were blinded to the
hypotheses of the study. All litters were scored only once in
the pre-weaning period at an age of the piglets of
5.5 ± 2.7 days (Mean ± SD).
Figure 1 Faces were scored as follows: 0, pale and pink skin, with bristles and without any deposit or efflorescence (a); 1, presence of oedema, exudation
and/or erosions (b). As soon as erosions were visible, face biting between piglets could not be ruled out.
Inflammation and necrosis syndrome in piglets
Statistics
The statistical evaluation was conducted on data from 19
herds, including 382 litters and 4725 piglets. Analysis of
traits was performed using the IBM SPSS (Version 23) soft-
ware package. Piglet data were aggregated by litter to pro-
vide the percentage of piglets per litter with alterations in the
form of inflammation/necrosis of the tail, ear base, heels,
coronary bands, teats and umbilicus, vulva, and face. The
statistical unit was the litter (n = 382). General data analysis
was performed using the descriptive function, based on the
mean, standard deviation, minimum and maximum. Effects
of sows’ and boars’ genetics were tested using the following
generalised mixed linear model, leading to least square
means:
μ = mean + HðS ´ BÞI + Sj + Bk + Dl + Am + eijklmn
where mean is the mean for the trait,
H(S × B)i = random effect of herds within genetics (boar after
sow); Sj the fixed effect of sow’s genetics, Bk the fixed effect
of boar’s genetics, Dl the fixed effect of degree of docking,
Am the age of piglets as covariate, eijklmn the error.
Residuals were tested and found to be distributed
approximately normally. Correlations were analysed as
Spearman correlations. Multiple testing was adjusted by
Bonferroni correction. Levels of significance was
P < 0.05.
The effects of intact tails (non-tail docked piglets) on the
outcome analysis were estimated for the following data
subset out of four herds with 83 litters (531 piglets in 45
litters with tails docked half; 337 piglets in 28 litters with 1/3-
docked tails; 94 piglets in 10 litters without tail docking,
respectively). The percentage of piglets with inflammation/
necrosis of the tail was analysed by univariate ANOVA, with
the herd as a random effect and the piglets’ age as a cov-
ariate. Data are presented as means and standard error. The
coefficient of determination for this model was 27%.
The effect of the piglet’s age was estimated as a random
factor in ANOVA.
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Reiner, Lechner, Eisenack, Kallenbach, Rau, Müller, Fink-Gremmels

Figure 2 Ear bases of piglets were scored as follows: 0, pale pink, with bristles and without any deposit or efflorescence (a); 1, presence of swelling,
erythema (b), exudation, encrustation or necrosis (c).

Table 1 Descriptive statistics for piglets showing clinical signs of an inflammatory response (in total, 4725 piglets, 350 litters, 19 herds)
Percentage of piglets affected in litters Percentage of litters affected in herds Percentage of herds affected

Inflammation of Mean SD Min Max Mean SD Min Max Mean

Heels 73.4 29.9 0 100 97.7 7.4 70 100 100

Coronary bands 54.1 28.4 0 100 97 6.7 80 100 100
Tail 11.3 16 0 90.9 53.7 27.4 0 90 94.7
Teats 4.3 9.8 0 58.3 22.4 32.9 0 90 42.1
Umbilicus 3.3 13.7 0 100 8.7 26.1 0 90 10.5
Ear base 0.5 2.9 0 30.8 3.2 6.9 0 45 10.5
Others
Face 16.3 23.4 0 90.9 45.9 37.4 0 100 79
Vulva swelling 0.2 2 0 18.2 1.6 6.9 0 30 5.3
Loss of tail1 0.02 0.4 0 7.7 0.01 0.03 0 13 10.5
Min = minimum; Max = maximum.
1
Only one of the piglets had lost its tail, probably by mechanical damage.

Results piglets could be affected by tail inflammation on distinct

herds (Table 2). The herd effect was statistically
Table 1 shows the descriptive statistics for piglets, litters and
significant for all clinical findings, explaining between 27%
herds. Piglets were affected by inflammation of the heels,
and 73% of the variance in the prevalence of lesions
coronary bands and docked tails in 73.4%, 54.1% and
(Table 2). A further 2% to 17% of variance was explained by
11.3% of cases. The other clinical findings were visible at
the sows’ genetics, whereas the boars’ genetics had only
lower rates. There was a clear variation between litters,
minor effects.
ranging from 0% to 100% of piglets affected. Almost all
litters were affected by inflammation of the heels and cor-
onary bands and more than 50% of the litters had at least Effects of degree of tail docking
one piglet with tail inflammation. These three When the prevalence of alterations within litters was asses-
dominant clinical findings were present in almost all herds sed, a negative correlation between docking length and the
(94.7% to 100%). Within herds, zero to 34.5% of the prevalence of tail lesions was noted. Litters with tails docked

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 Inflammation and necrosis syndrome in piglets

Table 2 Least square means, SD, minimum (Min) and maximum (Max) of the percentage of piglets in litters showing clinical signs of inflammation
(4725 piglets in 350 litters from 19 herds) and estimated variance explained by herd, sows’ genetics and boars’ genetics
Herds descriptive statistics Estimated variance (%) explained by

Clinical sign Mean SD Min Max Herd1 Sows1 genetics Boars1 genetics

Heel inflammation 73.4 25.5 18.5 99.5 0.69* 0.12* 0.00

Coronary band inflammation 54.4 19.8 26.0 97.0 0.45* 0.03* 0.00
Facial injuries 16.5 18.0 0.0 60.8 0.56* 0.08* 0.00
Tail necrosis 11.3 9.7 0.0 34.5 0.35* 0.14* 0.05*
Teat inflammation 4.3 6.8 0.0 20.2 0.45* 0.02 0.06*
Umbilical inflammation 3.4 12.1 0.0 51.9 0.73* 0.17* 0.07*
Ear base inflammation 0.5 1.7 0.0 7.3 0.31* 0.14* 0.01
Vulva swelling 0.2 1.0 0.0 4.5 0.27* 0.03* 0.01
1
Proportion of the variance explained by the respective effect in the total variance.
*Effect is statistically significant (P < 0.05).

Figure 3 Tail bases and tail tips of piglets were scored as follows: 0, pale pink, with bristles and without any lesions, deposit or efflorescence (a); 1, if
there were loss of bristles, swelling and discolouration (b), swelling, redness, erosion or coating (c), signs of inflammation at the tail base (d, e),
encrustation and/or necrosis at the tail tip (f). Within the scope of the study, inflammation/necrosis of the base or tip of the tail were aggregated to the
parameter inflammation/necrosis of the tail. There were no signs of bitten tails or mechanical destruction of tails.

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Reiner, Lechner, Eisenack, Kallenbach, Rau, Müller, Fink-Gremmels

Figure 4 Heels of piglets were scored as follows: 0, not swollen and free from cracks and signs of bleeding (a); 1, presence of swelling (b), internal
bleeding (c), cracks and separation from sole (d). Moreover, the dew claws could be involved.

Figure 5 Coronary bands of piglets were scored as follows: 0, not swollen and free from any lesions (a); 1, presence of clinical signs of inflammation like
swelling, redness or exudation (b), encrustation or necrosis (c). Moreover, the dew claws could be involved.

half showed the least occurrence of tail necrosis compared to tip-clipped tails (1/3 docked) and 68% of undocked piglets.
litters with 1/3-docked or undocked tails. Percentage of The differences between undocked piglets and those with
piglets affected by tail necrosis increased from 8.3% within docked tails were significant (P = 0.04 and P = 0.002 for tip
litters that were docked half to 14.8% of piglets with docked and half docked piglets, respectively) (Figure 9).

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 Inflammation and necrosis syndrome in piglets

Figure 6 Teats of the piglets were scored as follows: 0, not swollen and free from any deposit or efflorescence (a); 1, presence of swelling (b), redness (c)
or necrosis (d).

Figure 7 The umbilicus of each piglet was scored as follows: 0, not swollen and free from any signs of inflammation (a); 1, presence of swelling or
redness (b).

Figure 8 The vulva of female piglets was scored as follows: 0, not swollen and free from any signs of inflammation (a); 1, presence of swelling and
redness (b).

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Reiner, Lechner, Eisenack, Kallenbach, Rau, Müller, Fink-Gremmels

Figure 9 Effect of degree of tail docking on percentage of piglets per

litter affected by tail necrosis. Data were collected from four herds at
which all individual docking methods were employed: 531 piglets in 48
Figure 10 Effect of the age of piglets on the percentage of animals per
litters docked at the half (−1/2) tail length; 337 piglets in 28 litters with
litter, affected by inflammation of the heels and coronary bands and
tip docking (~ one-third of the tail cut) ( −1/3); 94 piglets in 10 litters
inflammation/necrosis of the tail (mean ± standard error). The correlation
without tail docking (0). Data show medians and boxplots (75%/25%
of piglet age with inflammatory alterations was statistically significant
percentiles) with whiskers (95%/5% percentiles). Significance was tested
(P < 0.001). Exact values are given as Supplementary Table S2.
with a median test. The overall effect of degree of tail docking was
significant at P < 0.001). The difference between −1/2 tail and 0 (not
docked) was significant at P = 0.002; the difference between −1/3 tail
and 0 was statistically significant at P = 0.04. Exact values are given as
Supplementary Table S1.

Effect of piglet age

Although piglets in individual herds and litters were scored at
different days of life, an overall trend analysis indicated that
the clinical signs increased during the 1st week of life and
then decreased again during the 2nd week (P < 0.001)
(Figures 10 and 11). Inflammation and necrosis of heels,
coronary bands and tails were already visible at days 1 and 2
of life, while the other clinical signs (inflammation of vulva
and ear base) started from days 2 or 3 onwards. Different
clinical signs showed significant, mostly positive correlations
with each other (Table 3).
Table 4 shows the impact of the genetics of sows and
boars on the assessed clinical signs. Besides the significant
effects of sow and boar, there was also a significant herd
effect for all assessed clinical signs (P < 0.001). The genetics
of the sow had a significant effect on inflammation and
necrosis of the tail (even though all tails were docked), claw
coronary bands, heels, teats, umbilica and ear base, as well
as on the prevalence of facial injuries. In particular, litters of
sows’ genetic G4 showed a higher overall susceptibility to
developing inflammation and necrosis in some parts of the
body of the piglets. Litters from the Pietrain boar line were
more prone to develop inflammation and necrosis of the tail,
heels, teats and ear base, but not to inflammation of the
coronary bands.
Discussion
The present study aimed to get insight into the prevalence of
clinically visible inflammatory processes in piglets in the first
days of life. The scoring system included a visual scoring of
inflammation and necrosis of the tail, ear base, claw cor-
onary bands and heels, as well as umbilical area and vulva in
Figure 11 Effect of the piglets’ age on the percentage of piglets per
litter, affected by inflammation/necrosis of teats, umbilicus, vulva and ear
base and by inflammation/injuries of the face (mean ± standard error).
The correlation of the piglet age was statistically significant (P < 0.001),
except for inflammation/necrosis of vulva and ear base. Exact values are
given as Supplementary Table S3.
piglets and is in line with current strategies in the assessment
of animal-based welfare indicators (see European Network of
Centres of excellence for Animal Welfare (ENCAW) report,
2016). Field observations and scientific studies have shown
that discontinuing tail docking under current practical con-
ditions can increase the prevalence of tail biting (Valros et al.,
2004; Lahrmann et al., 2017). While various factors may
induce tail biting (EFSA, 2007; D’ Eath et al., 2014), earlier
studies focussed on tail-biting as a behavioural disorder
attributable to the barren environment and housing condi-
tions. However, even under extensive outdoor conditions as
they are the common practice in Switzerland, a prevalence of
tail biting between 14% and 20% was recorded in 2004
(Walker and Bilkei, 2006). This suggests that three causalities
have to be distinguished: tail biting as a behavioural disorder
(also denoted primary biting; Taylor et al., 2010), and

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 Inflammation and necrosis syndrome in piglets

Table 3 Spearman correlations between percentage of piglets in litters affected by the respective clinical signs (350 litters)
Clinical signs Coronary band inflam Heel inflam Facial injuries Teat inflam Umbilical inflam Ear base inflam Vulva inflam

Tail necrosis 0.237* 0.177* 0.100 0.200* −0.067 0.106* 0.104

Coronary band inflammation 1 0.392* 0.282* 0.204* −0.118* 0.173* 0.127*
Heel inflammation 1 0.471* 0.420* −0.086 0.207* 0.102
Facial injuries 1 0.526* 0.252* 0.149* 0.105*
Teat inflammation 1 0.110* 0.224* 0.163*
Umbilicus inflammation 1 −0.060 −0.029
Ear base inflammation 1 −0.018
inflam = inflammation.
*P < 0.05.

Table 4 Least square mean and standard error for the effects of sows’ and boars’ genetics on the percentage of piglets in litters, affected by clinical
signs of inflammation (350 litters)
Sows’ genetics Boars‘ genetics

Clinical signs G1 G2 G3 G4 Pietrain Duroc

Tail necrosis 6.8 ± 2.6a* 7.3 ± 1.4a 17.7 ± 1.6b 10.6 ± 2.0a 13.5 ± 1.1a 5.9 ± 1.2b
Coronary band inflammation 53.4 ± 4.5a 51.0 ± 2.4a 55.0 ± 2.7a 67.9 ± 3.4b 55.4 ± 1.9 53.8 ± 2.0
Heel inflammation 90.5 ± 3.2a 69.6 ± 1.8b 60.4 ± 2.0c 96.6 ± 2.5a 77.5 ± 1.3a 71.0 ± 1.5b
Facial injuries 28.3 ± 3.4a 14.8 ± 1.8b 10.8 ± 2.0c 14.5 ± 2.6bc 18.3 ± 1.4 15.1 ± 1.5
Teat inflammation 6.1 ± 1.5b 3.6 ± 0.8a 3.3 ± 0.9a 7.3 ± 1.2b 6.5 ± 0.6a 0.8 ± 0.7b
Umbilical inflammation 0.0 ± 1.6a 12.8 ± 0.9b 0 ± 1.0a 0 ± 1.2a 1.0 ± 0.7a 8.6 ± 0.7b
Ear base inflammation 0.0 ± 0.5a 0.0 ± 0.3a 0.3 ± 0.33a 3.7 ± 0.41b 0.8 ± 0.2a 0.0 ± 0.2b
G1 to G4 = four different genetic lines of sows, representing typical production lines of various breeding companies.
Data represent least square means of the percentage of affected piglets per litter.
a,b,c
Between groups, means with different superscript letters differ significantly at P <0.05.

secondary biting of pre-damaged tails, where the victim
tolerates interactions with pen mates, due to a primary
inflammatory process resulting in ischemic tail lesions.
Moreover, tail necrosis without biting can be observed.
This third category of tail lesions occurs already in piglets
at a very early stage of life and without any interference from
other pigs (Penny et al., 1971; Santi et al., 2008). In these
cases, the authors described necrotic lesions at the base and
tip of tails in new-born piglets. They assumed circular vas-
cular constrictions and local ischemia as a possible patho-
genesis and emphasized that this type of lesions can be
clearly differentiated from tail biting. Penny et al. (1971)
described that tail necrosis started as an erythema at the
base of the tail of 4-day-old docked or undocked piglets,
which agrees with the findings of the present study.
Inflammation and necrosis of the tail, claw coronary bands
and inflamed heels have been detected in the current study
involving piglets during the 1st day of life (2 litters with 23
piglets). This makes a major influence of external factors such
as the housing conditions less likely and points towards a
metabolic, endogenous stressor and/or systemic challenge
from pro-inflammatory agents. Moreover, the obvious
improvement in the 2nd week of life, especially in the signs of
inflammation at the coronary bands and heels, supports this
consideration. Any mechanical cause (such as poor floor
conditions) would have led to a progression of the patholo-
gical alterations over time rather than the observed decrease
in the severity of the lesions as recorded in the current study
after day 6. The involvement of pathogens in the process
cannot be completely excluded, because no further diagnostic
investigations were conducted. However, none of the herds
had specific health problems at the time of the investigation.
Taken together, these findings support the hypothesis that
piglets regularly experience a generalized inflammatory
reaction that can be described as SINS. According to Lang-
bein et al. (2016), SINS, a syndrome that leads to inflam-
mation and necrosis in piglets, has to be regarded as
indicator of an impaired animal welfare.
The causal agents that induce this inflammatory syndrome,
however, remain to be elucidated. One of the most common
inducers of an inflammatory response is lipopolysaccharide (of
Gram negative bacteria, particularly Escherichia coli). Lipopo-
lysaccharide exposure may occur already during and shortly
after parturition, and is followed by activation of toll-like-
receptor 4 (TLR4)-receptors signalling and subsequent release
of pro-inflammatory cytokines (for review see, Vallance et al.,
2017). The interplay between psychosocial stress factors, an
inflammatory response and the vulnerability to infections in
piglets and the links to animal welfare were shown recently by
Tuchscherer et al. (2018).
The current results, which included also the analysis of a
possible correlation between the tail-docked and non-tail-
docked piglets clearly indicated the higher prevalence of tail
lesions in piglets with undocked tails. Although the cohort of

9
Reiner, Lechner, Eisenack, Kallenbach, Rau, Müller, Fink-Gremmels
undocked piglets was rather small in this study, these find-
ings require further investigation, considering the demand
(EU Directive 2008/120/EC) that routine tail docking of pig-
lets should be phased-out. No additional blood or tissue
samples were investigated to characterize the nature of the
clinically observable lesions. However, there was no evidence
of tail biting or other behavioural abnormalities in this age
group. Whether or not these findings can be related to the
prevalence of tail lesions during the fattening period remains
to be elucidated. Individual tail lesion reports from the
abattoir were not available for the scored piglets, but the
mean prevalence reported from the selected farms reached
30% in fatteners.
In conclusion, the current data which are based on clinical
investigations of individual suckling piglets show an unex-
pected high prevalence of inflammatory reactions in suckling
piglets. The onset of the clinical signs during the 1st days of
life, their combined appearance and the spontaneous
improvement during the 2nd week of life, largely exclude
commonly discussed causes such as physical injury induced
by poor housing conditions and undesirable behaviour such
as tail and ear biting. As the described clinical conditions
clearly indicate an impairment of animal welfare, further
studies should be devoted to identify the causative agents
including (subclinical) infectious disease and anti-nutritional
factors such as mycotoxins that are known to affect the
intestinal integrity and the innate immune system in the early
phase of life, thereby increasing the risk for an inflammatory
syndrome.
Acknowledgements
The authors would like to express their gratitude to the pig
farmers and their support during the scoring of the piglets at the
individual farms.
Declaration of interest
The authors declare that they have no competing interests.
Ethics statement
In the current study piglets were scored by visual inspection,
without applying any invasive intervention. The study was
conducted with the consensus of the responsible authorities
(Landesamt für Verbraucherschutz, Thuringia, Germany; AZ:
22.2684-04-07-001/16).
Software and data repository resources
None of the data were deposited in an official repository.
Supplementary materials
To view supplementary material for this article, please visit
https://doi.org/10.1017/S1751731118003403
10
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