How does PRRS affect intestinal health and performance of pigs?

What is PRRS and how does it affects intestinal health and productive performance of pigs? This review discusses the main characteristics of the disease.  It also reports experimental results, in which the perfomance of animals experimentally infected is compared with healthy counterparts. 

Porcine Reproductive and Respiratory Syndrome. What is PRRS?

Aetilogy

The virus of the porcine reproductive and respiratory syndrome (PRRSV) is the aetiological agent for the porcine reproductive and respiratory, grouped in the Nidovirales order, together with Coronaviridae, Roniviridae and Mesoniviridae.

History

The exact origins of PRRSV are still unknown. However, it appeared for the first time at the end of the 1980s, when USA veterinarians reported a mysterious disease causing reproductive problems in sows, as well as pneumonia/respiratory problems and suboptimal productive performance in all stages of production.

Esta enfermedad ha tenido varios nombres antes de denominarse como PRRS:

• La enfermedad misteriosa del cerdo
• Síndrome de infertilidad y respiratorio porcino
• Enfermedad de la oreja azul y el aborto epidémico porcino

Short after its discovery in the USA, the virus was detected in Europe. The European strains (type 1) and the European ones (type 2) were biologically and genetically different, having only 40 to 60% homology. Clinically, they share some signs; PRRS type 1 is generally produce reproductive disfunction, whilst type 2 produces both reproductive and respiratory signs.

Pathogenesis

Figure 1. Oronasal transmission.

In growing pigs, PRRSV produces a respiratory syndrome. The virus affects the lungs, targeting alveolar and intravascular macrophages and compromising their function. This results in the development of an interstitial pneumonia.

The viral infection increases the susceptibility of the lungs towards other pathogens (bacteria, viruses). However, the severity of the lung lesions could vary depending on different factors (virulence of the strain, pig genetics, environmental factors, etc.).

Clinical signs 

Clinical signs of respiratory PRRS include:

• Lethargy
• Reduced feed intake; anorexia
• Dyspnoea (breathing difficulties)
• Snizzing
• Coarse hair
• Fever
• Stunting

The maximum viremia of PRRS generally occurs 4- 7 days post-infection. Seroconversion is verified 7-21 days post-infection (Fig. 2).

Figure 2. Viremia (continuous line) and antibody response (dashed line) after PRRSV infection (dpi: days post infection.

PRRSV and pig perfromance

After the onset of the disease, pigs lose body condition and muscular mass; the hair becomes coarse. The disease can result in a 20% reduction in average weight gain during two to three weeks, and up to a 50% reduction in feed intake (Fig.3).

Figure 3. Impact of PRRS on general aspect (A) and loin size (B: longitudinal view; C: transversal section) at 17 days post-inoculation (dpi). 1: control (not infected); 2: caloric restriction (non-infected animal, consuming the same amount of feed as the infected animals); 3: Animals infected with PRRSV.  

The impaired performance of pigs due to PRRS can be explained by a reduction in feed intake, as shown in Figure 2, for non-infected animals consuming the same amount of feed as sick pigs (Treatments 2 and 3, respectively, in Figs. 3 and 4).

Figure 4. Effect of PRRS infection on body weight 16 days post inoculation (dpi)(dark-blue line), compared with non-infected, control pigs (green line) and non-infected pigs restricted to reach the feed intake of infected pigs (gray line).

Schweer et al. (2017) showed finishing pigs infected with PRRS take 14 days longer to get to market weight. (Fig. 5)

Figura 5. Differences in growth performance between female pigs challenged with PRRS (CHAL, in grey ) and control, non-infected animals (CONT, in green).

• Female pigs were challenged with PRRSV at 33.6 kg average body weight and taken to a target market weight of 128 kg.
• At day 0 (inoculation), one group of animals (CHAL) was intramuscularly inoculated with a live strain of PRSSV. The control group (CON) received saline solution (Schweer et al., 2017).

In the first 42 days post-inoculation (dpi), infected animals showed significant reduction in average daily gain (ADG), average daily feed intake (ADFI), and feed conversion efficiency (FCE), in comparison with control animals (Table 1).

Table 1. The effect of PRRS on average daily gain (ADG), feed intake (kg/day), feedconversion efficiency (FCE) between 0-42 dpi, 43-70 dpi, and from inoculation (0 dpi) and slaughter weight (128 kg at, approx., 114 dpi). 

Remarkably, during the second period (43-70 dpi), there were no significant differences in ADG, ADFI and FCE between inoculated and control animals.

In the experiment, infected animals ate less feed compared with the control animals (1.93 kg/d vs. 2.06 kg/d, respectively), and grew slower than their non-infected counterparts (0.80 kg/d vs. 0.90 kg/d, respectively). The FCE (weight gain/feed consumption) was not affected during the entire experimental period (1124 days).

Based on this study, and considering cost of extended housing time, feed intake, lower final body weight, and lower carcass value, the infection by PRRS has an estimated extra cost of, approximately, USD 10 per animal.

PRRS and its effect on intestinal function and integrity, and digestibility.

Depending on the PRRS virus type infecting the pigs, the performance can be affected by impaired ileal digestibility and total apparent digestibility of nutrients (Schweer et al., 2016a; Schweer et al., 2017; Schweer et al., 2018).There was also an alteration in the endogenous loss of basal amino acids and nitrogen in finishing pigs infected with PRRS, between 7 or 8 dpi and 18 or 19 dpi (Schweer et al., 2018).

Depending on the way intestinal health and integrity are evaluated, it was demonstrated that PRRS infections affect intestinal integrity and function (Schweer et al., 2016b)

• Between 7 and 8 dpi, significative reduction in endogenous losses of arginine, alanine, and proline were observed.
• Remarkably, basal endogenous nitrogen losses were reduced in pigs infected with PRRSV; however, total nitrogen losses throughout the digestive tract increased in infected animals.
• Between 18 and 19 dpi, there was an increasing tendency to the basal endogenous loss of threonine, whilst there was a reduction in the endogenous losses of arginine, alanine, and proline.

These data suggest that the basal endogenous losses in some amino acids are reduced during maximum viremia, and they were no different during the seroconversion period of PRRS pathogenesis. 

Figure 6. Histopathology of the intestinal mucosa in infected and non-infected pigs.

It was demonstrated that, in weaned piglets, the infection by PRRSV only has a minimal impact on the morphology and histopathology of the small intestine (duodenum, jejunum and ileum) (Fig. 6); infiltration with immune cells and villi fusion are two of the most common microscopic lesions. However, at 21 dpi, ex vivo mucosa permeability to macromolecules increased, together with active glucose transport and sucrase activity.

The data suggests that PRRS infection, on its own, may not necessarily have a negative effect on intestinal health and function.

Conclusions

• Depending on the type of virus (American or European), and its virulence, PRRS can affect animals in different ways.
• PRRSV infections may have a long-lasting effect on the health and performance of pigs, although intestinal function and digestibility may not be importantly affected.

This article was originally published nutriNews, with the title Cómo PRRS afecta al rendimiento, digestibilidad & salud intestinal?