Ohio State University Research/Extension Bulletin

Animal Sciences Research and Reviews

Special Circular 156

The Inflammatory Response in Selenium Deficient Chicks

A. Bartholomew^*, D. Latshaw^*, and D. Swayne⁺
^*Department of Animal Sciences and
⁺USDA/ARS Southeast Poultry Laboratory, Athens, GA

Summary

A selenium deficiency was produced in chicks. When the first chicks showed signs of exudative diathesis at 10 days of age, one deficient chick was injected with 1.5 g of selenium in 1 ml of water, one deficient chick was injected with 1 ml of water, and one selenium-adequate chick was injected with 1 ml of water. The two chicks injected with water were sampled after 2 days. Blood was drawn, the chicks were euthanized, and tissues were stored in formalin. The remaining chick was sampled after 6 days. Several trios were selected through 28 days of age, and the process was repeated. Selenium-deficient chicks had a dramatic increase in creative phosphokinase and leukocytes. Pectoral muscles had varying degrees of necrosis. By 6 days after selenium injection, many parameters had returned to normal. These results suggested an inflammatory response in selenium-deficient chicks.

Introduction

A selenium or vitamin E deficiency in chicks results in a condition called exudative diathesis. It is characterized by an accumulation of transparent fluid, usually around the breast. Tissue changes are similar to those of an inflammation, resulting in an accumulation of leukocytes and slight hemorrhaging. Capillary permeability is increased in the inflamed tissue. These effects have been attributed to oxidative damage to the capillaries. Damage is hypothesized to occur if the diet is deficient in selenium or vitamin E.

Methods and Materials

An experiment was designed to provide data about blood chemistry, hematology, and histology of chicks that were selenium-deficient or recovering from a deficiency. Chicks were hatched from eggs that were marginal in selenium and vitamin E. Approximately three-fourths of the chicks were fed a diet low in selenium and vitamin E, and the remainder were fed the same diet with 0.1 mg/kg added selenium. At 10 days of age, several chicks had developed exudative diathesis. Trios that were closely matched for severity were selected. One chick within a trio was injected subcutaneously with 0.5 ml of distilled water. The other two chicks in a trio were injected subcutaneously with 15 micrograms of selenite selenium in 0.5 ml of water. Some chicks that had been fed the selenium-supplemented diet were injected with 0.5 ml of distilled water.

Sampling began two days later. Blood was drawn from three chicks for hematological and chemistry studies. The chicks were then euthanized, and tissues were collected for histologic examination. One chick, originally selenium-deficient but injected with selenium, continued recovery for six days before sampling. This procedure occurred whenever a closely matched trio of chicks with exudative diathesis was identified.

Results

Results are not presented from chicks that were recovering from a selenium deficiency for only two days. Changes were evident, but in most cases criteria were not significantly different from those of the deficient chick. Histologic examination indicated damage to breast muscle and bone marrow. Myocyte necrosis in deficient chicks ranged from slight to severe. Six days after selenium injection, necrosis was uncommon, but fibrosis was extensive. Bone marrow from selenium adequate chicks had a myeloid-to-erythyroid ratio of 1.0. An increase in erythroid cellular elements changed the ratio in marrow from deficient chicks.

Several blood chemistry criteria were affected by the selenium status. Glucose, selenium concentration, and glutathione peroxidase activity were lower from selenium-deficient blood. The activity of several enzymes, including alanine transferase, aspartic transferase, and creatine phosphokinase, was increased.

Hematology also was altered by a deficiency. The hemoglobin content of red blood cells was decreased. Total leukocyte count in deficient chicks was more than double the number in selenium-adequate chicks (Table 1). The increase was due to a more than five-fold increase in heterophils. In addition, monocytes approximately tripled. Lymphocytes and basophils were less numerous from deficient chicks.

The change in leukocyte count indicates an inflammatory response and suggests a cause of exudative diathesis. Fluid accumulation and slight hemorrhaging might result from cytokines produced by leukocytes. Cytokines released at the site of injury facilitate adherence of immune system cells to vascular endothelial cells. Tissue necrosis factor, interleukin-1, and interleukin-6 act locally on endothelial cells to increase vascular permeability. This hypothesis provides an alternative explanation for the condition of exudative diathesis.

Table 1. Number of leukocytes (x 10⁹/L) as affected by selenium status.

Selenium status

Cell Adequate Deficient Corrected

(n=7) (n=6) (n=5)

Leukocytes 25.19^b 53.74^a 29.72^b

Lymphocytes 13.86^a 6.20^b 9.36^ab

Heterophils 7.19^b 40.05^a 13.04^b

Eosinophils 0.64^b 0.60^b 4.62^a

Basophils 1.56^a 0.12^b 0.88^ab

Monocytes 1.94^b 6.77^a 1.82^b

^ab Means in a row with different letters are significantly different (P < 0.05).

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Table 1. Number of leukocytes (x 10⁹/L) as affected by selenium status.
	Selenium status
Cell	Adequate	Deficient	Corrected
	(n=7)	(n=6)	(n=5)
Leukocytes	25.19^b	53.74^a	29.72^b
Lymphocytes	13.86^a	6.20^b	9.36^ab
Heterophils	7.19^b	40.05^a	13.04^b
Eosinophils	0.64^b	0.60^b	4.62^a
Basophils	1.56^a	0.12^b	0.88^ab
Monocytes	1.94^b	6.77^a	1.82^b
^ab Means in a row with different letters are significantly different (P < 0.05).