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Interpretive Summary: Thyroid hormone suppression in feeder pigs following polymicrobial or porcine reproductive and respiratory syndrome virus-2 challenge 

By: Dr. Emily Taylor

The swine industry continuously battles infectious disease challenges; unfortunately, the nature of our intensive management makes it particularly vulnerable. Understanding how the numerous physiological systems respond to disease is advantageous to scientists working to establish immunity. The endocrine system's role is poorly characterized, though it likely coordinates a portion of the complex disease resilience trait. The current study focused on thyroid hormones trying to understand their role in porcine disease response. 

Nursery-aged pigs were exposed to a natural polymicrobial disease challenge with an array of bacterial and viral pathogens. Thyroxin (T4) and triiodothyronine (T3) levels were measured and decreased significantly by 14 days post-exposure (DPE). However, T3 levels rebounded by 48 DPE, while T4 remained depressed. There was a positive correlation with T3 and T4 levels with acute and long-term average daily gain (ADG). In addition, authors sawt to establish the effect of porcine reproductive and respiratory syndrome virus (PRRSV)-infection on thyroid hormone levels. All animals presented with a decrease in both thyroid hormones reaching a minimum of 7 days post-inoculation (DPI) when challenged with one of two PRRSV2 strains but rebounded by 42 DPI. Groups with greater ADG had significantly greater T3 and T4 levels post-challenge. 

In conclusion, the results from the current study provide evidence that swine are particularly susceptible to disruption of the thyroid hormone system following disease challenge. The authors suggest investigating the role of thyroid hormones and phenotypes (growth rate, feed intake, and carcass quality) in the absence of disease to identify management or treatment strategies. In addition, determine if external manipulation of the relationship between thyroid hormone levels and pathogen replication during infection will compromise a vital component of the host-pathogen defense.

This article is now available in the Journal of Animal Science