1

A INFLUÊNCIA GENÉTICA SOBRE SAÚDE E BEM-ESTAR ANIMAL

Knap PW, Bloemhof S, Donisete do Nascimento J *
donisete@agroceres.com

1. INTRODUCTION
Animal health and animal welfare are both multi-dimensional characteristics. Many of the el-
ements that play a role here, are under some kind of genetic control. Pig breeding programs can
therefore make a positive contribution to animal health and animal welfare. This will require (1) re-
cording the relevant traits on pigs with known pedigree in commercial conditions, and (2) proper
statistical processing of those data into estimated breeding values, and (3) inclusion of those esti-
mated breeding values in the breeding goal and in the selection index.
In practice, the limiting factor will often be formed by point (1) above. "Recording the relevant
traits on pigs with known pedigree in commercial conditions" is usually a laborious and costly job,
and it must be done properly: with sufficient data volume, with a good distribution of the data
across farms or pens or other environmental factors, with a balanced distribution of the recorded
pigs across sire families, and as a routine activity over a long period. If not done properly, the re-
sulting estimated breeding values are very likely to be non-informative and genetic improvement
will not happen.
Given those limitations, in many cases it may be more efficient and effective to change ani-
mal management factors (such as nutrition, housing, and/or health care) than to look for a genetic
solution. But genetic improvement has the strong advantage that it is cumulative over time – so, if it
works it may eventually solve the whole problem.
2. ANIMAL HEALTH
In livestock production, animal health is influenced by three traits with a genetic background:
(i) disease resistance, (ii) disease tolerance, and (iii) infectivity, see Figure 1. Completely resistant
animals are able to keep the life cycle of the pathogen under control: when they get infected, they
can prevent the pathogen from multiplying itself in their body (often by killing it off) and as a result
they do not get sick. By contrast, when completely tolerant animals get infected the pathogen mul-
tiplies in their body, but they do not get sick and performance levels are not affected – one way or
another they have "learned to live" with the pathogen. The third trait, infectivity, quantifies how
many susceptible group mates will be infected by an infected individual. This is an important pa-
rameter in epidemiology, to study and predict disease transmission.
Important characteristics of these traits are: (1) in most cases they are not binary 0 / 1 traits
but continuous traits: animals are more or less resistant, and more or less tolerant, to most diseas-
es – but there are exceptions, see section 2.1; (2) resistant animals do not need tolerance, and
tolerant animals do not need resistance – so if there is selection for improved performance in infec-
tious conditions, then resistance and tolerance may become negatively correlated; (3) tolerant ani-
mals are not affected by the pathogen but at the same time they do not prevent it from multiplying –
as a result they may be very infectious ("super-spreaders") and may keep the disease going in the
population; (4) resistance (and also vaccination) places selection pressure on the pathogen, which
is likely to evolve in an attempt to neutralize it – and because microbes can evolve much faster
than vertebrates do, this co-evolution may indeed neutralize the increased resistance of the host;
(5) this does not hold for tolerance.
From resistance and tolerance combined follows resilience: "the ability to be productive in
spite of infection" (Stear et al., 2013), either by suppressing the pathogen (resistance) or by "living
around" it (tolerance) or a combination of both – in practical terms: the production performance lev-
el in infectious conditions without quantitative knowledge of pathogen load.
2.1 Classical selection
Recording the three basic traits (resistance, tolerance, infectivity) is difficult, to begin with
because they can only be measured in infectious conditions. So for animal breeding, recording
must take place outside the nucleus with its high biosecurity, and genomic prediction technology is
likely to play a crucial role. Resistance is the least challenging of the three traits to measure: identi-
fy animals that are infected with the pathogen of interest, and measure the pathogen load in their
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body (in terms of viremia, or antibody titer, or cytokine concentration, or fecal egg count, or similar
parameters) after a fixed number of days post-infection.
As mentioned above, resistance against a few specific pathogens is essentially under control
of just one gene in the host organism. Examples are Escherichia coli F18 and F4 in pigs (Vögeli et
al., 1997; Bertels et al., 1997), scrapie in sheep (Hunter et al. 1994), Marek virus in poultry (Maas
et al., 1981), and infectious pancreatic necrosis in Atlantic salmon (Moen, 2009; Houston, 2010).
Cases like these can be exploited relatively easily, and proper selection can lead to an almost
completely resistant population in a few animal generations.
But in most cases the genetic background is scattered across very many genes, each with a
small effect on resistance. A good example in pigs is in Figure 2 (data from Kreikemeier et al.,
2015) which shows the effect of 56433 DNA markers (SNPs, here combined into 2587 chromo-
some segments of 1 million nucleotides, holding on average 20 SNPs each) on the concentration
of the cytokine TNF-α after infection with the circovirus PCV2b that is responsible for diseases such
as PMWS. The combined genotypes of these SNPs explain 74 % of the phenotypic variance of the
trait (i.e. a very high heritability), but the most powerful single segment explains only 1.3 % of this
genetic variance and all the other ones are (far) below 0.5 %.
Similar polygenic patterns were found for resistance against the PRRS virus, but Boddicker
et al. (2014) detected an additional major gene. Rashidi (2016) detected that same gene in the
same pig population and also evaluated those pigs for tolerance to PPRS – his results are in Figure
3: the markers in the peak on chromosome 4 (associated with genes that induce cytokines) explain
22.7 % of the genetic variance of PRRS resistance, and there are other loci on chromosomes 9
and 11 that stand out from the rest somewhat. By contrast, PRRS tolerance shows a very polygen-
ic pattern in this population, with the most influential marker explaining only 4.2 % of the genetic
variance, and each of the rest (much) less.
Tolerance is much more difficult to measure than resistance. It is defined as a change: "the
change in performance as pathogen load changes" (Bishop & Woolliams, 2014), and it is therefore
most conveniently quantified as the linear regression of performance on pathogen load, within indi-
vidual animals (which will be extremely difficult) or within families, for example sire progeny groups
(which will require a lot of work, because each family will have to be large, and there will have to be
many families to make the statistics work properly). This requires (i) at least two measurements: at
a low and at a high pathogen load, (ii) quantification of the pathogen load each time, and (iii) ab-
sence of confounding the x-variable with the y-variable in the regression, via control of the relation
between initial host performance (before infection) and pathogen load. In many routine livestock
breeding programs this will be very laborious – the most realistic approach would then be via ge-
nomic prediction with regular renewal of the training population. Kause (2011) studied the required
data design and statistical methods for all this, and concluded that family size and x-y confounding
are the critical elements here. See also section 3.1.2 on reaction norms, below, which is the same
approach with pathogen load as the x-variable.
Although it will be very challenging to deal with disease tolerance in pig breeding, the trait is
important because of possible genetic antagonisms with resistance. If this genetic correlation is
negative, and resistance is gradually improved by selection, then tolerance will gradually go down
and as a net result resilience (i.e. production performance in infectious conditions, as above) may
not improve or even go down, particularly if the pathogen co-evolves successfully to neutralize the
improved resistance. And because tolerance is so difficult to measure, the fact that this correlation
is negative will usually be unknown. The literature gives very little clear information about this an-
tagonism; a good example of the possible level of uncertainty is in Figure 4 where tolerance of ma-
laria and tolerance of nematodes show completely opposite relationships with resistance to those
pathogens in inbred laboratory mouse strains.
Anacleto et al. (2018) describe a complicated experimental design that was required to
measure Philasterides dicentrarchi infectivity in Atlantic turbot. The most important conclusion from
that study is that infectivity is indeed a heritable trait in that species.
All this suggests that it is certainly possible to breed pigs specifically for improved disease
resistance, tolerance and/or infectivity, but it will require (i) very large volumes of very hard-to-
measure data, (ii) sophisticated statistical processing of that data, and (iii) a sound strategy to give
weighting to these possibly antagonistic traits in the breeding goal. Not easy.
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A much easier alternative would be to select directly for increased resilience, the net out-
come of resistance and tolerance. This requires recording of production traits in infectious condi-
tions (but it does not require quantification of the infection load), and using the data for breeding
value estimation of selection candidates in the nucleus. Because of nucleus biosecurity, recording
must take place on commercial farms and the pigs there must be close relatives of the nucleus se-
lection candidates – see section 3.1.1 for more detail. Mulder & Rashidi (2017) used computer
simulation to study how a resilience selection program influences the underlying traits resistance
and tolerance, and conclude that the outcome is uncertain, very much dependent on the correlation
structure, as described above.
Of course, much of the environmental challenge in commercial conditions is not due to infec-
tion load but to nutritional and housing factors, and with that we gradually move from animal resili-
ence to animal robustness (section 3.1.2).
2.2 Genome editing
A completely different way to approach improvement of disease resistance or tolerance is
through genome editing (Proudfoot & Burkard, 2017). A currently popular example is about com-
plete PRRS resistance in pigs, which was achieved through editing a particular segment of the
CD163 gene on pig chromosome 5, so that this gene is either knocked out completely (Whitworth
et al., 2016) or is modified in its active part (exon 7) that allows the PRRS virus to replicate itself in
the pig (Burkard et al., 2017; Yang et al., 2018). Because resistance is achieved in a single step
here, issues connected to a possible antagonism with tolerance (see section 2.1) do not apply
here.
An important issue here is that Figure 3 shows no significant signals on chromosome 5 at all
– this is because the pig's CD163 gene has no nucleotide variation ("polymorphism", in molecular
genetics) that is anyhow connected to PRRS resistance: in that respect the gene is fixed. Genome-
Wide Association Studies (GWAS) like the ones of Figures 2 and 3 detect association between (i)
the trait of interest (disease resistance or tolerance, in these cases) and (ii) DNA markers that ac-
tually have different alleles in the animal population (i.e. that are polymorphic). But when there is no
polymorphism then no association can be found, and the relevant gene will not be detected. In
such cases we need sound biological knowledge about the process of interest: in the PRRS case,
knowledge about the pig's CD163 protein and how the PRRS virus uses it for its replication (Van
Breedam et al., 2010) – and how that might be changed.
For the animal breeding sector this means that such knowledge must be obtained – in this
case from virologists and immunologists. That is perfectly possible and feasible, but for many
breeding companies it forms a completely novel approach that requires in-house expertise about
basic physiology and how to integrate it with the day-to-day running of a breeding program. Again,
not easy.
3. ANIMAL WELFARE
Intensive livestock production systems may lead to reduced animal welfare in three ways.
 Breeding goals with a lack of balance between production traits and animal robustness traits are
likely to cause fitness constraints – particularly in environmental conditions that are inadequate
to support the improved production potential.
 Intensive housing and management conditions shelter the animal from climatic, nutritional, par-
asitic and predatory challenges – but restrict much of the expression of its instinctive behavioral
repertoire ("deprivation", in ethology). This deprivation leads to frustration, with welfare prob-
lems for the affected individual and possibly for its penmates.
 Undesirable animal features are commonly reduced by routine invasive treatments such as
beak trimming in poultry, dehorning in cattle, or tail docking and castration in pigs – these are
pragmatic actions, but unrefined and never-ending, and painful for the animal. Many of those
undesirable features can also be dealt with through animal breeding: more complicated, but
permanent and better for animal welfare.
3.1 Robustness
When animals of high-performance genotypes are kept in production systems that are inad-
equate to provide the resources they need to express their performance potential, the animals may
show disturbed resource allocation and functional disorders of the skeletal and cardiovascular sys-
tems, of muscle physiology, of the reproductive system, or of the immune system. For pigs, obvi-
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ous indicators of reduced animal welfare in this respect are increased mortality rates, reduced sow
longevity, disease, and lameness.
The issue here is environmental sensitivity. The problem can be dealt with by making the
environment more resource-providing, and/or by making the genotype less sensitive. There are two
strategies for the latter: (i) direct selection for robustness traits, and (ii) selection against environ-
mental sensitivity as measured through reaction norms.
3.1.1 Selection for robustness traits
Livestock robustness can be defined as "the ability to combine a high production potential
with resilience to stressors, allowing for unproblematic expression of a high production potential in
a wide variety of environmental conditions" (Knap, 2005). The classical problem with this ability
occurs in the form of genetic antagonisms between production traits and robustness traits (Rauw,
1998; Knap & Rauw, 2009) – natural selection is not powerful enough to maintain (or improve) an-
imal robustness in intensive production systems; it must be supported by artificial selection. Genet-
ic antagonisms can be neutralized by using adequate selection criteria to select for an adequate
breeding goal. Earlier breeding goals were inadequate in this respect, as they did not include ro-
bustness traits (Goddard, 2009). A breeding goal should include all heritable traits that have an
impact on profitability (Gjedrem, 1972) – and mortality, morbidity and lameness certainly have such
an impact. Such traits can be included in the profit equation for pig production (Knap, 2009); this
provides marginal economic values, and these are required for inclusion in the breeding goal.
Various strategies for genetic improvement of piglet vitality and survival, leg soundness and
longevity, stress sensitivity, and disease resistance were summarized by Rydhmer & Lundeheim
(2008). These are hard-to-measure traits, mostly categorical (a few discrete classes) with low inci-
dences and relatively low heritabilities, so that large data volumes from challenging environments
are required for meaningful breeding value estimation. Their genetic improvement has benefited
considerably from BLUP and now benefits even more from genomic technology as shown by Knol
et al. (2016) in the following example.
Post-weaning mortality qualifies easily as a hard-to-measure trait: a binary (0 / 1) trait with
low incidence (p ≈ 0.05) and low heritability (h2 ≈ 0.05), strong and erratic environmental influences,
and cumbersome individual recording – but with a very high economic value (Knap, 2014). As men-
tioned in section 1, the main challenge here is proper data recording: any type of breeding value
estimation will require very high data volumes to achieve reasonable statistical power for such a
trait. The first requirement for breeding value estimation is always variation, and the variation of a
binary trait is proportional to its incidence: recall that its variance equals p×(1– p). Therefore, the
ideal farm for recording this trait is very large, has a high mortality incidence, continues with that for
a long time, and has staff strongly motivated toward high-quality data recording. Such farms are
difficult to find; they will necessarily be commercial production farms (as opposed to the breeding
company’s nucleus units), and the pigs will be crossbreds. To maintain a close genetic connection
to the nucleus selection candidates, the pigs will have to be produced by semen from nucleus AI
boars. Our example gives the mean reliability of the post-weaning mortality EBV for nucleus selec-
tion candidates, based on data recorded in such a system. Marker-Assisted selection was set up
for this trait in 2005, using 5 to 20 DNA markers in various lines; the resulting EBVs had an aver-
age reliability of 0.14. Genomic selection was implemented in 2010 using a dedicated small marker
panel, followed by single-step evaluation based on a routine 64k SNP chip in 2012. This genomic
EBV had an average reliability of 0.22, i.e. a 50 % increase of selection accuracy in animals at the
end of their performance test; for a binary trait with a 0.05 incidence and a ditto heritability, the reli-
ability value of 0.22 is equivalent to a progeny test on 101 progeny.
Figures 5, 6 and 7 show realized genetic improvement of leg soundness and mortality traits,
coinciding with improvement of production performance, in eight pig lines. This shows that it is per-
fectly possible to improve animal robustness together with increasing production potential. Notice
that the period reported here (2000 to 2009) was before genomics technology was introduced in
pig breeding – the critical element here is inclusion of all those traits in the breeding goal, and
proper data recording. That way, genetic antagonisms between production and robustness traits
can be neutralized. Genomic selection only makes it more feasible.
3.1.2 Reaction norms
When progeny of specific sires are (i) identified as such, (ii) spread across a wide environ-
mental range (e.g. through AI), and (iii) recorded for a production trait, their production performance
 5

can be related to a descriptor of the environment (e.g. a herd-year-season effect) by linear regres-
sion. This should produce a positive slope overall: better environments lead to better production.
When the regression is performed separately for sire progeny groups, and if there is genetic varia-
tion in environmental sensitivity of the trait's production potential, this produces regression lines
("reaction norms", in population genetics) with different intercepts and slopes for different sire fami-
lies. The intercepts are equivalent to the conventional EBVs for the trait. The slopes quantify an
animal's requirements for environmental support of its genetic potential – they detect robustness
as defined above: sires with a steeper slope produce progeny that are less robust.
Friggens & Van der Waaij (2008) discuss how selection for increased production levels (i.e.
for high reaction norm intercepts) may cause a gradual increase of environmental sensitivity (i.e. of
the slopes). Knap & Su (2008) confirmed this in terms of a strongly positive genetic correlation be-
tween intercept and slope of reaction norms for litter size in pigs. The slopes have a very low herit-
ability in that data, so the increase of environmental sensitivity would be very slow. This presents
another example of genetic antagonisms, which can be neutralized by including both the intercept
and the slope of the reaction norm of each production trait in the breeding goal and in the selection
criterion. Knap (2005) presents a way to calculate their marginal economic values.
These are demanding statistics. Knap and Su (2008) analyzed their data in three consecu-
tively larger subsets. The medium subset held more than 50,000 sows – comparable to the largest
litter size datasets in the scientific literature of that time. Still, its parameter estimates for the reac-
tion norm slopes differed considerably from those from the largest dataset with more than 120,000
sows, and the accuracy of its slope estimates was too low to be useful in practical breeding. The
smallest subset held more than 30,000 sows, but its parameter estimates were clearly unrealistic
and not significantly different from zero. Similar issues hold for the required environmental range in
the data. Not easy, again.
3.2 Behavioral deprivation
Intensive housing and management systems often restrict the expression of instinctive be-
haviour patterns ("motivations", in ethology) of the pig: foraging, rooting and exploring in all age
classes, and nest-building in sows. This happens because intensive housing environments do not
provide the required space or substrates. Something similar holds for deprivation of social contact
in individually housed sows, where the "required substrate" is other pigs. This results in frustration,
leading to redirected behavior (stereotypies) or apathy.
Again, the most efficient and effective way to solve such problems would often be to adapt
the housing system. Three genetic alternatives have been described, as follows.
First: the obvious way would seem to be direct selection against stereotypies and apathy –
this will not be very difficult in large crate-housed sow systems but on the longer term it may actual-
ly increase the problem because the redirected behaviour serves as an outlet for frustrated motiva-
tions, and as such forms the animal's final way to deal with the load of the stressor. Reducing it
would create a system under stress (with its negative consequences for homeostasis and produc-
tion) without any security valve.
Second: selection for passive or active strategies to cope with stress. Coping strategies have
been intensively studied in laboratory mouse and rats, and also in humans; this requires knowledge
of the neuro-endocrinology of the stress axis, the hypothalamus-pituitary-adrenal (HPA) axis (see
Martínez-Miró, 2016). Chronic stress can cause a persistent overproduction of corticosteroids by
the HPA, which can damage neuro-receptors in the brain. Interaction with the sympathetic nervous
system leads to active versus passive coping strategies. These traits are heritable: mouse and rat
populations have been successfully selected into both directions. Actively and passively coping
pigs differ in terms of how the hypothalamus regulates the pituitary: via CRH in passive copers, and
via vasopressin in active copers (Karman, 2003). But in both cases, corticosteroid production is
increased and neuro-receptors are damaged, so selection for any particular coping strategy will not
be a good solution in pig breeding.
Third: focus on the regulation of the HPA axis at its very beginning, i.e. regulation of the hy-
pothalamus which is done by the limbic system of amygdala and hippocampus (Morris, 2006). This
part of the brain also regulates emotional and cognitive functions, and has been described as the
central link between stress and declarative learning. In livestock this type of learning occurs during
adaptation to housing facilities, milking regimes etc. (Manteuffel, 2002; Gimsa et al. 2018). Ge-
nomic techniques would be very useful for detecting the responsible genes (e.g. Terenina et al.
 6

2012) and based on that for modifying the pig's instinctive patterns, so that the motivation for be-
havior that cannot be supported by the production system would be reduced. This would extend
9000 years of pig domestication, which always has been a process of reducing the animal's drives
for exploration, aggression, etc (Knap, 2012).
3.3 Dominance aggression
Another issue of intensive production systems is avoidance of dominance aggression, par-
ticularly when pigs are being mixed into new groups (Jensen, 1994; Couret et al., 2009): confine-
ment prevents animals from avoiding aggressors: they cannot run away from them. Such behaviour
has significant genetic components (Turner et al., 2009), possibly connected to the coping strate-
gies described in section 3.2. The main factor that would complicate selection against such behav-
iour is the difficulty of data recording (see section 3.4.2), which makes genomic selection an inter-
esting option again.
3.4 Avoidance of invasive treatments
There is an increasing societal drive to reduce painful treatments such as castration and tail
docking of piglets; both issues are under intensive debate in Europe right now. The question is then
which genetic options there are to reduce the reasons why those treatments are performed: (i) boar
taint and (ii) tail biting.
3.4.1 Boar taint
Boar taint is an unpleasant odour of pig meat. It occurs in 1–10 % of entire males (depend-
ent on many nutritional and animal management factors: Hortós et al., 2015) and it is caused by
several chemical components, most importantly androstenone (a sex hormone and pheromone)
and skatole (a metabolite of the gut microflora). Skatole is normally broken down in the liver, but
the enzyme that does this is inhibited by high circulating levels of androstenone. Tissue concentra-
tions of both components are variable, line-specific and heritable, so that it is feasible to select pigs
for reduced boar taint levels. The relevant genes are gradually being identified. Figure 8 gives an
example of the typical distribution of the EBVs of these two traits: the vast majority of animals have
a low (i.e. favorable) EBV for both components, with a strong correlation between them. At the
higher (i.e. unfavorable) end, the variation in both components is much wider and the correlation
between them is much weaker. The best genetic strategy is then to construct an index of both
EBVs and select against high values of that index.
3.4.2 Harmful social behaviour
Tail biting is a form of harmful social behaviour ("social" because it involves other pigs) in in-
tensive animal production, possibly a form of redirected foraging behaviour as in section 3.2;
D'Eath et al. (2014, their Figure 1) describe the considerable complexity of this trait in terms of
stocking density, pen climate, dietary imbalance and feeder capacity, and substrate availability.
Other forms of harmful social behaviour are ear biting in pigs, vulva biting in group-housed sows,
piglet savaging by sows, and feather pecking in poultry.
Like in section 3.2, the obvious way to deal with tail biting genetically would be to simply se-
lect for shorter tails; but this is not a good idea, for two reasons.
First: tail length is a direct function of the number of caudal vertebrae, and this is linked to
the number of dorsal and lumbar vertebrae, in the back of the animal. Correlated changes there are
likely to reduce the number of pork chops per pig, and may in the longer term lead to similar con-
genital anomalies (spina bifida, rear leg paralysis, incontinence, and in homozygotes embryonic
death) as described for tailless cats and dogs with mutations in the T-Box Brachyury gene that
have also been described in sheep (Hytönen et al., 2009; Buckingham et al., 2013; Zhi et al.,
2018).
Second: the core of the problem is not in the tail of the recipient / victim but in the brain of the
actor / performer, and possibly also in the brain of the recipient. The frustrated performer pig has to
look for an outlet for its frustration, and finds it in redirected foraging behavior – and the victim pig
tolerates this instead of moving away from it at an early stage. Brunberg et al. (2016) distinguish
between performers, victims and neutral animals (which are not involved in harmful social behavior
either way), and suggest that performers and victims represent the two extremes (hyper-active or
hyper-passive) of a continuum of strategies to cope with the intensive housing environment,
whereas neutral animals are successful copers either because they have a mixed coping strategy
or because they are better adapters in general. Wilson et al. (2012) performed a GWAS like in our
 7

Figures 2 and 3, and detected a few significant signals both for the "performer" status and for the
"victim" one.
In group housing, an individual's phenotype for any trait (growth rate, mortality, etc.) is influ-
enced by its own direct breeding value for the trait and the associative breeding values of its pen-
mates, positive or negative ("indirect genetic effects": Bijma et al., 2007). This principle has been
worked out in detail for growth rate and feed intake in growing pigs (e.g. Chen et al., 2008;
Bergsma et al., 2008); associative effects can contribute large parts of the heritable variance in
those traits. Intuitively, the same should hold for social behavior traits.
Van der Zande (2017) applied this method to tail biting records and found a heritability of
0.24, 70 % of which was due to "performer" effects and 6 % was due to "victim" effects. Much ear-
lier, Breuer et al. (2005) used conventional statistical methods to estimate heritabilities for tail biting
in two pig populations (both with a performer incidence of about 3 %) at 0.00 and 0.05 on the ob-
served scale – so the indirect genetic effects approach seems much more effective to detect genet-
ic variation. A very useful aspect of this approach is that the phenotype to be recorded is not the
observed act of tail biting as such (i.e. spotting the performer, which is difficult and time-consuming)
but the presence of a damaged tail: the "victim" effect is the direct genetic effect, the "performer"
effect is the indirect one in this analysis. The disadvantage of the method is that it can only work if
each pig in a particular pen has close relatives (e.g. full sibs or half sibs) distributed across many
other pens, so that each of the penmates of a victim can be checked for having relatives in other
pens with a victim – if that is the case, then the "performer" EBV of each of those relatives is in-
creased. Again, not easy in terms of performance test design.
4 CONCLUSIONS

It follows from all the above that it is possible to create genetic improvement in animal health and
animal welfare. Many of the traits involved are heritable and can be recorded, so that breeding val-
ues of selection candidates can be estimated and incorporated in the routine selection indexes at
the nucleus level. The limiting factor in practically all the cases described above is data recording –
in many of these cases this will be so difficult and/or laborious that improvement of the nutritional,
housing and/or infectious environment may be the more efficient and more effective solution.
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Figure captions:

Figure 1. The main genetic (G), environmental (E) and phenotypic (P) elements that play a role in
the relation between production potential and health in livestock. Modified from Knap & Bishop
(2000; Figure 1).

Figure 2. Associations of 56433 DNA markers (SNPs, here combined into 2587 chromosome seg-
ments of 1 million nucleotides, holding on average 20 SNPs each) on the concentration of the cyto-
kine TNF-α in pigs, after infection with circovirus PCV2b. Horizontal axis: position of each segment
in the genome, chromosomes are color-coded. Vertical axis: proportion of the genetic variance of
the trait explained by each segment. Data (not the graph itself) from Kreikemeier et al. (2015; Table
S1); segments with a zero association are not plotted.
 10

Figure 3. Associations of 44787 DNA markers (SNPs) with resistance (left: AUC14 = the area un-
der the viremia curve up to 14 days post infection) and with tolerance (right: the regression coeffi-
cient of y = average daily gain up to 28 days post infection, on x = AUC14) of pigs to the PRRS
virus. Horizontal axis: position of each SNP in the genome, chromosomes are color-coded. Vertical
axis: –log(P) = –1 times the logarithm of the P-value of a genome-wide significance test for the as-
sociation of each SNP (larger values represent stronger significance). The horizontal reference line
at –log(P) = 5.41 indicates a 20 % False Discovery Rate for the resistance trait. Modified from Ra-
shidi (2016; Figures 5.2 and 5.5).

Figure 4. Tolerance (vertical axes) in relation to resistance (horizontal axes) to malaria (left: modi-
fied from Råberg et al., 2007, Figure 3) and to a nematode (right: data from Athanasiadou et al.,
2015) among inbred mouse strains.

Figure 5. Ten-year genetic trends of growth rate and leg soundness in the same eight pig lines.
Notice that both traits improve simultaneously in each line. The color coding differs from Figures 6
and 7.

Figure 6. Ten-year genetic trends of total number born, farrowing survival rate and preweaning sur-
vival rate in the same four pig lines. Notice that all three traits improve simultaneously in each line.
The color coding differs from Figures 5 and 7.

Figure 7. Ten-year genetic trends of lean tissue growth rate, feed conversion ratio and total (from
farrowing to slaughter) mortality rate in the same eight pig lines. Notice that all three traits improve
simultaneously in each line. The color coding differs from Figures 5 and 6.

Figure 8. Estimated breeding values for the subcutaneous fat content of the boar taint compounds
androstenone and skatole in a single pig line.