Immunoassay of serum ferritin is currently used to evaluate the clinical iron status of human beings, horses, cattle, and swine. Because ferritins are immunologically species specific, a separate assay must be developed for each species. We have developed an ELISA for serum ferritin in dogs, using a monoclonal anti-canine ferritin antibody. Ferritin standards were linear (r = 0.997) from 0 to 80 ng/ml. Recovery of ferritin from canine serum was 94%. Dilutions of pooled canine serum were linear from 0 to 50% (r = 0.994). Within-assay coefficient of variability was 5.5%, whereas assay-to-assay coefficient of variability ranged from 12.5 to 21%. This assay should provide a nonsurgical means of accurately estimating dogs' iron stores.

A study was undertaken to determine the pressor and toxic effects of etoposide, an antineoplastic agent, when administered IV in 0.9% sodium chloride solution (0.4 mg of etoposide/ml) over a 30-minute period to dogs at a dosage of 40 mg/m2 of body surface. On day 1, 6 adult German Shorthaired Pointers were anesthetized with halothane, and blood pressures were measured via a femoral artery catheter before, during, and after the etoposide was administered. Systolic, diastolic, and mean blood pressures of each dog increased significantly (P less than 0.01) within 30 minutes after initiation of etoposide infusion. On day 3, when the dogs were not anesthetized, etoposide was again administered to each dog, using the same dosage. Each dog developed a moderate to severe cutaneous reaction characterized by moderate to severe pruritus, urticaria, and swelling of the head and extremities that began during the second infusion of etoposide. These same cutaneous reactions were seen on day 30, when etoposide was administered to 3 of the previously treated dogs and 2 previously untreated Beagles. We concluded that the administration of the commercial preparation of etoposide is likely to cause a significant reduction in blood pressure of anesthetized dogs, and that the drug is likely to induce a moderate to severe cutaneous reaction when administered to unanesthetized dogs.

Ureterocolonic anastomosis was evaluated in 13 clinically normal dogs. Urinary continence was maintained after surgery, and the procedure was completed without technique errors in all but 2 dogs. Three dogs died within 5 weeks (2 of undetermined causes and 1 of aspiration pneumonia and neurologic disease), and 1 dog was euthanatized 4 months after surgery because of neurologic signs. Two healthy dogs were euthanatized 3 months after surgery for light microscopic evaluation of their kidneys. Five dogs were euthanatized 6 months after surgery for light microscopic evaluation of their kidneys. Gastrointestinal and neurologic disturbances developed in 4 dogs at various postoperative intervals. Plasma ammonia concentration measured in 2 dogs with neurologic signs was increased. Plasma ammonia concentration measured in 5 dogs without neurologic signs was within normal limits. All 5 dogs, in which metabolic acidosis was diagnosed, had high normal or above normal serum chloride concentration. Serum urea nitrogen values were increased after surgery because of colonic absorption of urea. Serum creatinine concentration was increased in 1 dog 6 months after surgery. Individual kidney glomerular filtration rate was reduced in 38% (3/8) of the kidneys from 4 other dogs at 6 months after surgery. Of 5 dogs euthanatized at 3 to 4 months after surgery, 4 had bilateral pyelitis, and 1 had unilateral pyelonephritis. Six months after surgery, pyelonephritis was diagnosed in 40% (4/10) of the kidneys from 5 dogs. The ureterocolonic anastomosis procedure is a salvage procedure that should allow complete cystectomy. However, variable degress of metabolic acidosis, hyperammonemia, and neurologic disease may result.

On each day of feeding on susceptible calves, salivary glands obtained from groups of adult ticks that transmitted Anaplasma marginale were examined for A marginale colonies by use of light microscopy and transmission electron microscopy. On day 8 of feeding, salivary glands were examined, using fluorescein-labeled antibody and methyl green-pyronine stain. Use of fluorescein-labeled antibody consistently revealed small numbers of fluorescent foci in salivary gland acinar cells obtained from ticks that had fed for 8 days. Colonies of A marginale were seen by transmission electron microscopy only in salivary gland acini of male ticks; these colonies could not be identified, using light microscopy, in companion 1-micron plastic sections stained with Mallory stain. Methyl green-pyronine stain, used commonly to detect theilerial parasites in tick salivary glands, did not differentiate A marginale from cytoplasmic inclusions normally found in salivary gland acinar cells.

Neutralizing and nonneutralizing antibodies to bovine viral diarrhea (BVD) virus were detected in 3 cows persistently infected with noncytopathic BVD virus after vaccination with modified-live cytopathic BVD virus. Neutralizing antibodies detected in serum samples from each persistently infected cow at 3 weeks after vaccination were highly specific for certain isolates of cytopathic BVD virus and reacted only with a viral protein with a molecular weight of 53,000. Neutralizing antibodies to 1 of 3 isolates of noncytopathic BVD virus were detected in a serum sample obtained at 12 weeks after vaccination from 1 of 3 persistently infected cows. Nonneutralizing antibodies were detected in all cows at 7 to 12 weeks after vaccination.The nonneutralizing antibodies were less specific for isolates of BVD virus and reacted with viral proteins with molecular weights of 115,000, 80,000, 53,000, and 47,000.

A reproducible model of postweaning colibacillosis was obtained by controlling management and environmental variables to simulate conditions often seen at weaning. Suckling pigs were exposed briefly to starter diet at 1 week of age, weaned at 3 weeks of age, held at an ambient temperature of 20 +/- 2 C, again given the starter diet. One day after weaning, each pig was given 10(10) colony-forming units of enterotoxigenic Escherichia coli strain M1823B (0157:K88ac:H43-LT+ STb+) in broth containing 1.2% sodium bicarbonate via stomach tube. In vitro adhesion by strain M1823B to isolated intestinal branch borders was used to tst pigs for susceptibility to K88. In this model, 3 syndromes were induced in susceptible pigs: (1) peracute fatal diarrhea; (2) moderate diarrhea, weight loss, and fecal shedding of the inoculum strain; and (3) no diarrhea, weight loss, and fecal shedding of the inoculum strain. Rotavirus particles were not found in fecal specimens of pigs with diarrhea. The K88-susceptible, noninoculated control pigs remained clinically normal. It was concluded that susceptibility to adhesion by K88+ enterotoxigenic Escherichia coli was a requirement for the production of disease in this model; inoculation with rotavirus was not necessary.

Three Beagles with chronic anemia and reticulocytosis were studied. The dogs originated from a large breeding colony and appeared clinically normal with the exception of splenomegaly. The PCV ranged from 30 to 39% (normal, 46 to 56%), with reticulocyte indices of 2.3 to 9.9. Red blood cells were morphologically normal, and examination of marrow aspirates revealed erythroid hyperplasia. Shortened chromium-51 RBC life-spans (7.2 to 15.4 days in anemic dogs; 22.2 to 25.2 days in control dogs) documented a hemolytic anemia. Acquired causes of hemolytic anemia were ruled out. Red blood cells had normal glycolytic enzyme activities, no evidence of unstable or abnormal hemoglobin, and had altered osmotic fragility curves. The breeding of 2 anemic dogs resulted in off-spring with anemia and reticulocytosis. Polyacrylamide gel electrophoresis revealed no abnormalities in RBC membrane cytoskeletal proteins in all anemic adult dogs and in 3 offspring.