Metabolic insights and background from naturally affected pigs during Streptococcus suis outbreaks

Author:

Fabà Lluís1ORCID,Aragon Virginia234,Litjens Ralph1,Galofré-Milà Núria234,Segura Mariela5,Gottschalk Marcelo5,Doelman John1

Affiliation:

1. Trouw Nutrition R&D , Amersfoort 3811 MH , The Netherlands

2. Unitat mixta d’Investigació IRTA-UAB en Sanitat Animal. Centre de Recerca en Sanitat Animal (CReSA), Campus de la Universitat Autònoma de Barcelona (UAB) , Bellaterra, 08193, Catalonia , Spain

3. IRTA. Programa de Sanitat Animal. Centre de Recerca en Sanitat Animal (CReSA), Campus de la Universitat Autònoma de Barcelona (UAB) , Bellaterra, 08193 Catalonia , Spain

4. OIE Collaborating Centre for the Research and Control of Emerging and Re-Emerging Swine Diseases in Europe (IRTA-CReSA) , Bellaterra, Barcelona , Spain

5. Faculty of Veterinary Medicine, Swine and Poultry Infectious Disease Research Centre, University of Montreal , Saint-Hyacinthe, QC , Canada

Abstract

Abstract Streptococcus suis (S. suis) is an endemic zoonotic pathogen still lacking adequate prevention in pigs. The present case study looked back to the occurrence and consequences of S. suis outbreaks in our swine research facilities in search of new metabolic and physiological insight. From a series of outbreaks, a dataset was created including 56 pigs sampled during disease detection based on clinical signs. Pigs suspected with S. suis infection were defined as diseased (n = 28) and included pigs defined as neurologically diseased (n = 20) when severe neurological signs (central nervous system dysfunctions, i.e., opisthotonos, ataxia, and generalized tremor) were observed. Another set of 28 pigs included respective pen mates from each case and were defined as control. Representative deaths were confirmed to be caused by S. suis. Tonsillar swabs were collected and analyzed by quantitative polymerase chain reaction (qPCR) for total bacteria, total S. suis, and S. suis serotypes (SS) 2 (and/or 1/2) and 9. Blood and sera were analyzed to quantify blood gases, minerals, and S. suis reactive immunoglobulins against current isolates. Data collected included litter sibling associations, birth and weaning body weight (BW), and average daily gain (ADG) 7 d after the disease detection. In general, the disease increased pH, sO2 and the incidence of alkalosis, but reduced pCO2, glucose, Ca, P, Mg, K, and Na in blood/serum compared to control. The SS2 (and/or SS1/2) prevalence was significantly (P < 0.05) increased in neurologically diseased pigs and its relative abundance tended (P < 0.10) to increase in tonsils. In contrast, the relative abundance of total S. suis was lower (P > 0.05) in diseased pigs than control pigs. Levels of S. suis reactive IgG2 were lower, but IgM were higher (P < 0.03) in neurologically affected pigs compared to control. Furthermore, there was an increased proportion of sibling pigs that were diseased compared to control. In conclusion, our results evidence that naturally affected pigs were associated to average performing pigs without any predisease trait to highlight but a sow/litter effect. Besides, neurologically affected pigs had increased S. suis (SS2 and/or 1/2) prevalence and relative abundance, a respiratory alkalosis profile, and mineral loss.

Funder

Trouw Nutrition R&D

Centre de Recerca en Sanitat Animal CReSA

Publisher

Oxford University Press (OUP)

Subject

General Veterinary,Animal Science and Zoology

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