Evidence map›Paper›PMID 36860185›Full record

ArticleJournal of animal science2023

The genetic basis of swine inflammation and necrosis syndrome and its genetic association with post-weaning skin damage and production traits.

Natália Galoro Leite, Egbert Frank Knol, Stefanie Nuphaus, Roos Vogelzang, Shogo Tsuruta, Margit Wittmann, Daniela Lourenco

Open access · hybridAbstract read
In one paragraph

Article in Journal of animal science, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
9.1field-weighted citation impact, top 2% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

13 citing papers in PubMed, 28 citations in OpenAlex.

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  13. GWAS reveals genomic associations with swine inflammation and necrosis syndrome.Mammalian genome : official journal of the International Mammalian Genome Society · 2023
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 3 institutions in 3 countries.

Natália Galoro LeiteDepartment of Animal and Dairy Science, University of Georgia, Athens, GA 30602, USA.ORCID 0000-0001-9327-426X
Egbert Frank KnolTopigs Norsvin Research Center, Beuningen, GE 6641 SZ, The Netherlands.
Stefanie NuphausTopigs Norsvin Research Center, Beuningen, GE 6641 SZ, The Netherlands.
Roos VogelzangTopigs Norsvin Research Center, Beuningen, GE 6641 SZ, The Netherlands.
Shogo TsurutaDepartment of Animal and Dairy Science, University of Georgia, Athens, GA 30602, USA.ORCID 0000-0002-6897-6363
Margit WittmannFachhochschule Südwestfalen, Iserlohn, NRW 58644, Germany.
Daniela LourencoDepartment of Animal and Dairy Science, University of Georgia, Athens, GA 30602, USA.
Topigs Norsvin (Netherlands) · NLUniversity of Georgia · USSouth Westphalia University of Applied Sciences · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The swine inflammation and necrosis syndrome (SINS) is a syndrome visually characterized by the presence of inflamed and necrotic skin at extreme body parts, such as the teats, tail, ears, and claw coronary bands. This syndrome is associated with several environmental causes, but knowledge of the role of genetics is still limited. Moreover, piglets affected by SINS are believed to be phenotypically more susceptible to chewing and biting behaviors from pen mates, which could cause a chronic reduction in their welfare throughout the production process. Our objectives were to 1) investigate the genetic basis of SINS expressed on piglets' different body parts and 2) estimate SINS genetic relationship with post-weaning skin damage and pre and post-weaning production traits. A total of 5,960 two to three-day-old piglets were scored for SINS on the teats, claws, tails, and ears as a binary phenotype. Later, those binary records were combined into a trait defined as TOTAL_SINS. For TOTAL_SINS, animals presenting no signs of SINS were scored as 1, whereas animals showing at least one affected part were scored as 2. Apart from SINS traits, piglets had their birth weight (BW) and weaning weight (WW) recorded, and up to 4,132 piglets were later evaluated for combined skin damage (CSD), carcass backfat (BF), and loin depth (LOD). In the first set of analyses, the heritability of SINS on different body parts was estimated with single-trait animal-maternal models, and pairwise genetic correlations between body parts were obtained from two-trait models. Later, we used four three-trait animal models with TOTAL_SINS, CSD, and an alternative production trait (i.e., BW, WW, LOD, BF) to access trait heritabilities and genetic correlations between SINS and production traits. The maternal effect was included in the BW, WW, and TOTAL_SINS models. The direct heritability of SINS on different body parts ranged from 0.08 to 0.34, indicating that reducing SINS incidence through genetic selection is feasible. The direct genetic correlation between TOTAL_SINS and pre-weaning growth traits (BW and WW) was favorable and negative (from -0.40 to -0.30), indicating that selection for animals genetically less prone to present signs of SINS will positively affect the piglet's genetics for heavier weight at birth and weaning. The genetic correlations between TOTAL_SINS and BF and between TOTAL_SINS and LOD were weak or not significant (-0.16 to 0.05). However, the selection against SINS was shown to be genetically correlated with CSD, with estimates ranging from 0.19 to 0.50. That means that piglets genetically less likely to present SINS signs are also more unlikely to suffer CSD after weaning, having a long-term increase in their welfare throughout the production system.

Indexed as

ParturitionSwine DiseasesAnimalsBirth WeightBody WeightFemaleInflammationNecrosisPhenotypePregnancySwineWeaningbehaviorgenetic correlationheritabilitypigtail-bitingwelfare

Identifiers

PMID36860185
PMCPMC10050931
OpenAlexW4322757399

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.