Effect of progressive cachectic parasitism and growth hormone treatment on hepatic 5'-deiodinase activity in calves.

Thyroid status is compromised in a variety of acute and chronic infections. Conversion of thyroxine (T(4)) into the metabolically active hormone, triiodothyronine (T(3)), is catalyzed by 5'-deiodinase (5'D) mainly in extrathyroidal tissues. The objective of this study was to examine the effect of protozoan parasitic infection (Sarcocystis cruzi) on hepatic 5'D (type I) activity and plasma concentrations of T(3) and T(4) in placebo- or bovine GH (bGH)-injected calves. Holstein bull calves (127.5+/-2.0 kg BW) were assigned to control (C, ad libitum fed), infected (I, 250,000 S. cruzi sporocysts per os, ad libitum fed), and pair-fed (PF, non-infected, fed to intake of I treatment) groups placebo-injected, and three similar groups injected daily with pituitary-derived bGH (USDA-B-1, 0.1mg/kg, i.m.) designated as C(GH), I(GH) and PF(GH). GH injections were initiated on day 20 post-infection (PI), 3-4 days prior to the onset of clinical signs of the acute phase response (APR), and were continued to day 56 PI at which time calves were euthanized for liver collection. Blood samples were collected on day 0, 28, and 55 PI. Alterations in nutritional intake did not affect type I 5'D in liver. Treatment with bGH increased (P<0.05) 5'D activity in C (24.6%) and PF (25.5%) but not in I calves. Compared to PF calves, infection with S. cruzi reduced 5'D activity 25% (P<0.05) and 47.8% (P<0.01) in placebo- and bGH-injected calves, respectively. Neither nutrition nor bGH treatment significantly affected plasma concentrations of T(4) and T(3) on day 28 and 55 PI. However, plasma thyroid hormones were reduced by infection. On day 28 PI, the average plasma concentrations of T(3) and T(4) were reduced in infected calves (I and I(GH)) 36.4% (P<0.01) and 29.4% (P<0.05), respectively, compared to pair-fed calves (PF and PF(GH)). On day 55 PI, plasma T(3) still remained lower (23.7%, P<0.01 versus PF) in infected calves while plasma T(4) returned to control values. The data suggest that parasitic infection in growing calves inhibits both thyroidal secretion and extrathyroidal T(4) to T(3) conversion during the APR. After recovery from the APR, thyroidal secretion returns to normal but basal and bGH-stimulated generation of T(3) in liver remains impaired.