Porcine Reproductive and Respiratory Syndrome virus reduces feed efficiency, digestibility, and lean tissue accretion in grow-finish pigs.

Porcine reproductive and respiratory syndrome (PRRS) virus is a major swine virus that causes reproductive impairment in sows, as well as respiratory disease, reduction in growth rates, and mortalities in all ages of pigs. The objective of this study was to quantify the impact PRRS has on grower-finisher pig feed efficiency and tissue accretion rates. Thirty PRRS naïve, littermate pairs of maternal line Choice Genetics gilts (33.6 ± 0.58 kg BW) were selected and pairs split across 2 barns consisting of 5 pens (n = 6 pigs/pen per barn). Pigs in both barns were fed corn-soybean-DDGS diets ad libitum. All pigs in one barn were inoculated (CHAL) via an i.m. injection of a live PRRS strain isolated from the region (0 d post inoculation, dpi), while pigs in the other barn were given a saline control injection (CONT). Pig performance (ADG, ADFI, G:F) was assessed from 35 kg BW until each group reached market BW (128 kg). Additionally, longitudinal apparent total tract digestibility (ATTD) and body composition was assessed using Dual-energy X-ray absorptiometry (DXA) post inoculation (dpi) to estimate lean, protein, fat and bone accretion rates. Serological data from CHAL pigs showed that PRRS titers peaked 7 dpi and these pigs seroconverted by 35 dpi. According to both genomic and protein PRRS titers, CONT pigs were naïve to CHAL throughout the study. The PRRS infection reduced (P < 0.001) ATTD of dry matter, energy and nitrogen by 3 to 5% at 21 dpi and the reduction in ATTD persisted after 65 dpi. Compared to the CONT, CHAL pigs had decreased ADG (0.89 vs. 0.80 kg/d, P < 0.001), ADFI (2.05 vs. 1.93 kg/d, P < 0.001), and G:F (0.44 vs. 0.41 kg/d, P < 0.001) over the entire test period. The CHAL pigs also had attenuated DXA predicted whole body accretion of lean (547 vs. 633 g/d, P = 0.001), protein (109 vs. 126 g/d, P = 0.001) and fat (169 vs. 205 g/d, P = 0.001) compared to their CONT counterparts from dpi 0 to 80. Based on carcass data at slaughter (and consistent with the DXA data), CHAL pigs had leaner carcasses and reduced yields. These data clearly demonstrate that PRRS infection reduces digestibility, feed efficiency and protein accretion rates in grower-finisher pigs.

The effect of porcine reproductive and respiratory syndrome virus and porcine epidemic diarrhea virus challenge on growing pigs I: Growth performance and digestibility.

Porcine reproductive and respiratory syndrome (PRRS) and porcine epidemic diarrhea (PED) are two diseases costly to the U.S. swine industry. The objective of this study was to determine the impact of PRRS virus and PED virus, alone or in combination, on growth performance, feed efficiency, and digestibility in grower pigs. Forty-two gilts (16 ± 0.98 kg BW) naïve for PRRS and PED were selected and allocated to 1 of 4 treatments. Treatments included 1) a control, 2) PRRS virus infected, 3) PED virus infected, and 4) PRRS+PED coinfection (PRP). Pigs in treatments 2 and 4 were inoculated with a live field strain of PRRS virus via intramuscular and intranasal routes at 0 d after inoculation (dpi). Treatments 3 and 4 were orally inoculated with a cloned PED virus at 15 dpi. Infection with PRRS virus was confirmed by quantitative PCR and seroconversion. Infection with PED virus was confirmed with PCR. Control pigs remained PRRS and PED virus negative throughout the study. All pigs were offered, ad libitum, a standard diet with free access to water. During the test period, PRRS reduced ADG and ADFI by 30 and 26%, respectively ( < 0.05), compared with control pigs, whereas PRP decreased ADG, ADFI, and G:F by 45, 30, and 23%, respectively ( < 0.05). Additional reductions in ADG and G:F were detected in PRP pigs compared with singular PED or PRRS treatments (33 and 16%, respectively). The impact of PED, alone or in combination, on performance (15-21 dpi) reduced ADG (0.66 vs. 0.35 vs. 0.20 kg/d; < 0.01), ADFI (1.22 vs. 0.88 vs. 0.67 kg/d; = 0.003), and G:F (0.54 vs. 0.39 vs. 0.31; = 0.001) compared with control pigs. Compared with control pigs, PRRS infection did not reduce apparent total tract digestibility (ATTD) of nutrients and energy. However, PED infection, alone or in combination, decreased ATTD of DM and energy by 8 and 12%, respectively ( < 0.05). Compared with control pigs, PRP reduced N and OM ATTD by 13 and 3%, respectively ( < 0.05). No significant differences in apparent ileal digestibility (AID) were detected between virus challenges. However, Lys AID tended to be reduced in both PED treatments compared with the control (10 and 12%; = 0.095). Altogether, PRRS reduced growth but did not alter digestibility. Pigs challenged with PED and, to a greater extent, the coinfection of PED and PRRS viruses had reduced ADG, ADFI, G:F, and ATTD of nutrients and energy.

The effect of porcine reproductive and respiratory syndrome virus and porcine epidemic diarrhea virus challenge on growing pigs II: Intestinal integrity and function.

The objective of this study was to determine if intestinal function and integrity is altered due to porcine reproductive and respiratory syndrome (PRRS) virus and porcine epidemic diarrhea (PED) virus infection in growing pigs. Forty-two gilts (16.8 ± 0.6 kg BW), naïve for PRRS and PED, were selected and randomly assigned to 1 of 4 treatments: 1) a control (CON; = 6), 2) PRRS virus challenge only (PRRS; = 12), 3) PED virus challenge only (; = 12), or 4) coinfection of PRRS + PED viruses (PRP; = 12). Treatments 2 and 4 were inoculated with a live field strain of PRRS virus on d 0 after inoculation. Treatments 3 and 4 were inoculated with PED virus on 14 d after inoculation (dpi) and all pigs were euthanized 7 d later (21 dpi). Infection with PRRS virus was determined by viremia and seroconversion. Fecal quantitative PCR was used to confirm PED virus infection. Control pigs remained PRRS and PED virus negative throughout the study. Compared with the CON, intestinal morphology was unaffected by PRRS. As expected, PED and PRP treatments resulted in duodenum, jejunum, and ileum villus atrophy compared with the CON treatment ( < 0.01). Ex vivo transepithelial electrical resistance (TER) did not differ between CON and PRRS pigs (P < 0.05) but was reduced by 40% in PED alone ( < 0.01). Interestingly, TER was increased ( < 0.01) in the PRP pigs. Active transport of glucose was increased in PRRS pigs over CON pigs ( < 0.01), whereas PED had pigs increased ( < 0.01) active glutamine transport over the CON pigs. Jejunum GLUT2 mRNA abundance and sucrase, maltase, and Na+/K+ adenosine triphosphatase activities tended to be increased in PRRS pigs compared with CON pigs ( < 0.06). The jejunum AA transporter, SLC6A14, and mucin 2 mRNA abundance tended to be increased in PED-only pigs ( < 0.10). These data suggest that PRRS infection supports a higher affinity for glucose uptake, whereas PED favors glutamine uptake. Interestingly, digestive machinery during PED challenge remained intact. Altogether, PED but not PRRS challenges alter intestinal morphology and integrity in growing pigs.