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SUMMARY

Four 1-year-old steers were each inoculated orally with 10,000 Toxoplasma gondii oocysts of the GT-1 strain and euthanatized on postinoculation days (pid) 350, 539, 1191, and 1201. Samples (500 g) of tongue, heart, semimembranosus and semitendinosus muscles (roast), intercostal muscles (ribs), longismus muscles (tenderloin), brain, kidneys, liver, and small intestine were bioassayed for T gondii by feeding to cats and examination of cat feces for shedding of oocysts. Toxoplasma gondii was recovered by bioassays in cats from the 3 steers necropsied pid 350, 539, and 1191, but not from the steer euthanatized on pid 1201. Cats shed oocysts after ingesting tongue from 2 steers, heart from 3 steers, liver from 2 steers, and roast, ribs, brain, and intestines from 1 steer each. Toxoplasma gondii was not isolated from any of the other bovine tissues. In addition to tissues bioassayed in cats, homogenates of mesenteric lymph nodes, lungs, spinal cord, spleen, and eyes were bioassayed in mice for T gondii infection. Toxoplasma gondii was not recovered from the 135 mice inoculated with tissue from each of the 4 steers. All 4 inoculated steers developed high T gondii antibody titers (≥ 1:8,000) in the agglutination test, using formalin-fixed whole tachyzoites. In the steer euthanatized on pid 1201, agglutinating T gondii antibody titers decreased from 1:4,000 to 1:320 between 2 and 5 months after inoculation and to 1:20 by 19 months after inoculation.

Free access
in American Journal of Veterinary Research

mandibular and mesenteric lymph nodes of both cats were moderately to markedly large, and the normal appearance was distorted by friable pinpoint yellow-white nodules. The parenchyma of the spleen, liver, and lungs contained multiple white, round, raised

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in Journal of the American Veterinary Medical Association

the abdomen (12.4 × 10.5 × 11.7 cm). On the left lateral radiographic view, the mass silhouettes with the caudoventral aspect of the spleen ( Figure 2 ) and is superimposed with the small intestine. The small intestine is displaced to the right by the

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in Journal of the American Veterinary Medical Association

-needle aspirates of the spleen by comparing those results with histologic diagnoses. Additional information about underlying disease and ultrasonographic appearance was also obtained. Criteria for Selection of Cases Medical records from 247 dogs and cats in

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in Journal of the American Veterinary Medical Association

the esophageal wall was thickened ( Figure 1 ). The spleen was markedly enlarged (weight, 20 g [approx 3% of the ferret's body weight; normal spleen weight is 0.5% to 1.3% of a ferret's body weight]), had rounded edges, and was soft, pale, and mottled

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in Journal of the American Veterinary Medical Association

abnormalities except mild enlargement of the spleen. A nasogastric tube was passed and no net reflux was obtained, but the gastric contents were mixed with a small amount of blood. No current signs of colic were observed. Initial bloodwork revealed a PCV of 32

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in Journal of the American Veterinary Medical Association

Abstract

Objective—To determine whether a group of 3 genetic differences in the nonstructural protein (NS1) or 1 genetic difference in the structural protein (VP2) of Aleutian disease parvovirus (ADV) is responsible for an increase in the in vivo replication and pathogenicity of G/U-8, a chimera of ADV-G (nonpathogenic) and ADVUtah (pathogenic), compared with G/U-10.

Animals—32 eight-month-old female sapphire mink (Mustela vison).

Procedure—Chimeric viruses were constructed, propagated in vitro, and used to inoculate mink. Antiviral antibody responses, presence of serum viral nucleic acid, and serum gamma globulin concentrations were monitored for 120 days following inoculation. Histologic examination of the liver, kidneys, spleen, and mesenteric lymph nodes was performed after necropsy.

Results—A chimera containing only the 3 amino acid substitutions in NS1 did not elicit measurable responses indicative of replication or pathogenicity in inoculated mink. Serum antiviral antibody responses, frequency of detection of viral nucleic acid in serum, gamma globulin response, and histologic changes in mink inoculated with chimeras containing a valine residue at codon 352 (352V) of VP2 capsid were increased, compared with values from mink inoculated with chimeric viruses that did not contain 352V.

Conclusion and Clinical Relevance—A valine residue at codon 352 in the VP2 capsid protein of ADV affects in vivo viral replication and pathogenicity. This amino acid may be part of an incompletely defined pathogenic determinant of ADV. Further characterization of the pathogenic determinant may allow future development of focused preventive and therapeutic interventions for Aleutian disease of mink. (Am J Vet Res 2001;62:1658–1663)

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in American Journal of Veterinary Research

Abstract

Objective—To evaluate cyclooxygenase isozyme distribution in tissues from dogs and determine the differential sensitivity of canine cyclooxygenase (COX)-1 and -2 isozymes to nonsteroidal anti-inflammatory drugs (NSAIDs).

Sample Population—Canine tissue samples (stomach, duodenum, ileum, jejunum, colon, spleen, cerebral cortex, lung, ovary, kidney, and liver) were obtained from 2 dogs for northern and western blot analyses, and blood for whole blood COX assays was obtained from 15 dogs.

Procedure—11 NSAIDs were evaluated to determine their COX-2 selectivity in whole blood assays. The concentrations of the drug needed to inhibit 50% of enzyme activity (IC50) were then calculated for comparison. Expression and tissue distribution of COX isozymes were determined by northern and western blot analysis.

Results—Aspirin, diclofenac, indomethacin, ketoprofen, meclofenamic acid, and piroxicam had little selectivity toward COX isozymes, whereas NS398, carprofen, tolfenamic acid, nimesulide, and etodolac had more than 5 times greater preference for inhibiting COX-2 than COX-1. All canine tissues examined, including those from the gastrointestinal tract, coexpressed COX-1 and -2 mRNA, although protein expression was observed only for COX-1.

Conclusions and Clinical Relevance—Canine COX-2 was selectively inhibited by etodolac, nimesulide, and NS398; tolfenamic acid and carprofen also appeared to be preferential COX-2 inhibitors in dogs. The roles of COX-1 as a constitutive housekeeping enzyme and COX-2 as a proinflammatory inducible enzyme (as determined in humans) appear to apply to dogs; therefore, COX-2-selective inhibitors should prove useful in reducing the adverse effects associated with nonselective NSAIDs. (Am J Vet Res 2004;65:810–818)

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in American Journal of Veterinary Research

Abstract

Objective—To determine the effects of continuous low-dose infusion of lipopolysaccharide (LPS) on the expression of E-selectin and intercellular adhesion molecule-1 (ICAM-1) mRNA and neutrophil accumulation in the lungs, liver, spleen, small intestine, and pancreas in dogs.

Animals—11 healthy adult Beagles.

Procedure—Dogs received a continuous infusion of a low dose (10 µg/kg/h, IV) of LPS ( Escherichia coli055:B5) or saline (0.9% NaCl) solution (20 mL/kg/h, IV) for 8 hours. Activity levels of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and interleukin-6 (IL-6) and the number of WBCs in circulation were examined before and 1, 2, 4, and 8 hours after the onset of LPS infusion. Expression of E-selectin and ICAM-1 mRNA and the number of neutrophils in each tissue were examined.

Results—After the onset of LPS infusion, serum TNF-α and IL-1β activities transiently increased. Thereafter, IL-6 activity increased, and high IL-6 activity was maintained throughout the experiment. In dogs in the LPS group, expression of E-selectin mRNA increased only in the lungs, and expression of ICAM-1 mRNA increased in the lungs and liver; the number of neutrophils in the tissue increased in the lungs and liver.

Conclusions and Clinical Relevance—Results suggested that expression of E-selectin and ICAM-1 mRNA increased during sepsis, particularly in the lungs and liver, and that this increase was associated with neutrophil accumulation. Hence, inhibiting the activation of endothelial cells in the lung and liver may decrease organ damage caused by accumulated neutrophils and help regulate multiple-organ dysfunction. (Am J Vet Res 2005;66:1259–1266)

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in American Journal of Veterinary Research

Abstract

Objective—To characterize clinical and hematologic responses in dogs following experimental inoculation with Babesia gibsoni-like isolates from infected dogs in Oklahoma.

Design—Prospective study.

Animals—6 mixed-breed dogs.

Procedure—2 dogs were inoculated with organisms from a naturally infected dog, and 3 were inoculated with organisms from a second naturally infected dog (1 of these 3 dogs was splenectomized 1 week prior to inoculation). One dog was not inoculated. Complete blood counts were performed weekly.

Results—In the 5 dogs inoculated with organisms, parasites were initially detected 1 to 5 weeks after inoculation, and severity of parasitemia peaked with 1.9 to 6.0% of RBC infected by 4 to 6 weeks after inoculation. Parasitemia was easily detectable (> 0.1% of RBC infected) for 3 to 4 weeks. Clinical abnormalities included lethargy, fever, and pale mucous membranes but were mild to nearly inapparent in 2 dogs. All dogs developed regenerative anemia and marked thrombocytopenia. Thrombocytopenia developed before and lasted longer than the parasitemia. Profound but transient neutropenia was detected in some dogs. The splenectomized dog developed more severe parasitemia and anemia and more pronounced clinical abnormalities. Three dogs with intact spleens recovered without treatment.

Conclusions and Clinical Relevance—Results suggest that 2 or more genotypically distinct, but morphologically identical, small Babesia parasites can infect dogs in the United States. Compared with infection with small Babesia parasites from California, infection with these isolates resulted in less severe parasitemia and clinical abnormalities. Parasitemia was transient, indicating that identification of organisms in blood smears may be difficult in some dogs. (J Am Vet Med Assoc 2002;220:185–189)

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in Journal of the American Veterinary Medical Association