Effect of Infections on the Thyroid Gland.

Abstract

Cole, Womack and Gray 1 and others^2,3 described certain pathologic changes in thyroids of persons who suffered from acute or chronic infections, such as pneumonia or peritonitis. The glands were obtained at autopsy from individuals who succumbed to either an acute or chronic infection. The changes noted in the thyroid were of a two-fold nature, depending in each case on the acuteness or chronicity of the infection from which the patient died. Thus, where death was a result of pneumonia or acute peritonitis, the changes in the thyroid consisted mainly in desquamation of the epithelium lining the acini and softening of the colloid. When death of the individual was due to a more chronic type of infection, the thyroid did not show any epithelial desquamation, but rather a heaping up of the acinar cells with papillary projections into the alveoli, and increased scar formation. Very similar changes to those described above, were previously noted by Cole and Womack 2 in dogs in whom they had experimentally produced acute infections and toxemias.

We thought it of interest to carry out similar experiments in guinea pigs, because the thyroid gland of guinea pigs has been very carefully studied in the laboratory under normal as well as under various experimental conditions and we are therefore well acquainted with the changes which take place in the thyroid of guinea pigs under various conditions.

We used 26 guinea pigs, in 16 of which an acute infection was produced by injecting fecal material into the peritoneal cavity. The time of development of an acute peritonitis and the consequent death of the injected animal was found to vary according to the quantity of injected material and site of injection. If the site of injection was high up in the abdomen, viz., in the region of the diaphragm, where absorption is more rapid, the animal died much sooner than when injected in the pelvis.