Microcytosis is a common laboratory finding in dogs with congenital portosystemic shunt (PSS), although its pathogenesis is not yet understood. Because the most common cause of microcytosis in dogs is absolute or relative iron deficiency, iron status was evaluated in 12 young dogs with PSS. Complete blood counting was done before surgical correction in all dogs, and in 5 dogs after surgery, by use of an automated hematology analyzer. Serum iron concentration and total iron-binding capacity (TIBC) were determined colorimetrically, and percentage of transferrin saturation was calculated. Erythrocyte protoporphyrin content was quantified by use of front-face fluorometry. Serum ferritin concentration was measured by use of ELISA. Serum ceruloplasmin content was determined colorimetrically (with p-phenylenediamine dihydrochloride as substrate) as an indirect indicator of subclinical inflammation, which may result in impaired iron utilization. Special stains were applied to liver (10 dogs; Gomori's) and bone marrow aspiration biopsy (7 dogs; Prussian blue) specimens for qualitative assessment of tissue iron content. Nonpaired Student's t-tests were used to compare serum iron concentration, TIBC, percentage of transferrin saturation, and erythrocyte protoporphyrin, ferritin, and ceruloplasmin concentrations in dogs with PSS with those in clinically normal dogs. All dogs had microcytosis before surgery; microcytosis resolved in 3 dogs after surgical correction. Serum iron concentration and TIBC were significantly lower, in PSS-affected dogs than in clinically normal dogs. Erythrocyte protoporphyrin, ferritin, and ceruloplasmin concentrations in PSS-affected dogs were not significantly different from those in healthy dogs. Excess iron was not detected consistently in liver or bone marrow samples. These results suggest that relative iron deficiency, perhaps associated with altered iron transport and not absolute iron deficiency, is related to microcytosis in dogs with PSS.

Effects of selenium (Se) deficiency and supplementation on production of colostral immunoglobulins by beef cows and transfer of antigen-specific and nonspecific immunoglobulins to their calves were examined. Eighty beef cows, with marginal to deficient Se status (blood Se concentration, 50 micrograms/L), were allotted by breed and age to 1 of 4 Se treatment groups (n = 20/group): no supplemental Se; parenteral administration of 0.1 mg of Se and 1 mg of vitamin E/kg of body weight; ad libitum consumption of 120 mg of Se/kg of salt-mineral mix (SMM); and parenteral administration of 0.1 mg of Se and 1 mg of vitamin E/kg plus ad libitum consumption of 120 mg of Se/kg of SMM. All cows were inoculated IM with lysozyme. Cows consumed Se-deficient pastures or hay (21 to 62 micrograms/kg) during the study that began at mid-gestation and ended at postpartum hour 24. Although the concentration of specific lysozyme antibodies was not affected, cows given 120 mg of Se/kg of SMM (treatments 3 and 4) had higher colostral IgG concentration (P < 0.002) than did Se-deficient cows (treatments 1 and 2). Calves from cows in treatments 3 and 4 had higher postsuckle serum concentrations of IgG (P < 0.01) than did calves from cows in treatments 1 and 2. Colostral IgM and calf serum IgM concentrations did not differ among treatments.