Search Results

You are looking at 101 - 110 of 910 items for :

  • Refine by Access: All Content x
Clear All

retract the spleen to expose its hilus. Beginning at the splenic tail, the vessel-sealing device was used to seal and divide the splenic hilar vasculature immediately adjacent to the splenic parenchyma. Following completion of the splenectomy, the single

Free access
in Journal of the American Veterinary Medical Association

immediately submitted for necropsy. The body of the spleen contained a 6.5 × 7 × 4-cm, multilobulated, mottled yellow-tan to dark red mass ( Figure 1 ). On the capsular surface of all hepatic lobes, there were numerous, clearly delineated, slightly raised

Full access
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)

Full access
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)

Full access
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)

Full access
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)

Full access
in Journal of the American Veterinary Medical Association

Abstract

Objective—To determine the efficacy (durations of remission and survival) of an alternating-day radiation protocol for incompletely excised histologic grade-III solitary mast cell tumors (MCTs) in dogs.

Design—Retrospective study.

Animals—31 dogs.

Procedure—Radiation (52 Gy in an 18-fraction alternating-day protocol) was delivered to an area bordered by margins ≥ 3 cm around the surgical scar and to the associated local-regional lymph nodes. Dogs were not given chemotherapeutic agents concurrently or after radiation. Information on signalment, duration of remission, and survival time was obtained from medical records.

Results—Median and mean durations of remission were 27.7 and 17.0 months, respectively (range, 1 to 47 months). Median and mean durations of survival were 28 and 20 months, respectively (range, 3 to 52 months). Dogs with tumors located on the skin of the pinna, perineum, and prepuce had a median duration of remission greater than dogs with tumors located at other sites (27.7 and 14.4 months, respectively). Dogs with tumors ≤ 3 cm in maximum diameter before surgery survived longer than dogs with tumors > 3 cm (31 and 24 months, respectively). The remission rate was 65% and survival rate was 71% at 1 year after treatment. Sixteen dogs that were euthanatized had complications associated with local-regional tumor progression. Systemic metastases to liver, spleen, intestine, and bone marrow were detected in 1 dog.

Conclusions and Clinical Relevance—Without further treatment, incompletely excised grade-III mast cell tumors have high local-regional recurrence; local-regional treatment with radiation may effectively be used to manage many such tumors. (J Am Vet Med Assoc 2004;224:79–82)

Full access
in Journal of the American Veterinary Medical Association

Abstract

Objective

To evaluate stable rough mutants derived from Brucella melitensis 16M and B suis 2579 (biovar 4) as vaccines against homologous and heterologous Brucella spp in the BALB/c mouse model.

Design, Animals, and Procedure

Rough mutants VTRM1 and VTRS1 were obtained from B melitensis 16M and B suis 2579, respectively, by allelic exchange of the rfbU gene encoding mannosyltransferase with a Tn5-disrupted rfbU gene. Mice were vaccinated with VTRM1 or VTRS1 and challenge exposed 8 weeks later.

Results

VTRM1 and VTRS1 replicated extensively in the spleen during the first 3 weeks of infection, then decreased rapidly. Antibodies specific for the O polysaccharide were not detected in sera of mice inoculated with either rough strain. Vaccination with VTRM1 or VTRS1 induced protection against virulent strains of B abortus (2308), B melitensis (16M), B suis biovar 1 (750), and B suis biovar 4 (2579). VTRM1 also protected against B ovis (PA) and against 4 field isolates of B abortus from bison or elk. VTRS1 conferred protection against 4 field isolates of B suis biovar 4 from reindeer. Vaccines prepared from live VTRM1 or VTRS1 provided significantly greater protection than that afforded by vaccines of killed cells in QS- 21 adjuvant. Vaccination with VTRM1 containing VTRS1 gave minimal protection against the antigenically unrelated Listeria monocytogenes, thus demonstrating the immunologic specificity of protection against Brucella spp.

Conclusions and Clinical Relevance

Results encourage evaluation, in primary host species, of VTRM1 and VTRS1, along with RB51, as alternative vaccines to strain 19, Rev 1, or other smooth phase vaccines. (Am J Vet Res 1996; 57:677–683)

Free access
in American Journal of Veterinary Research

Abstract

Objective

To characterize the pathogenic potential of a unique Borrelia isolate obtained from a dog from Florida (FCB isolate).

Design

Prospective experimental infection.

Animals

32 preweanling Swiss Webster mice and 12 adult male Hartley guinea pigs were injected intraperitoneally with 105 spirochetes.

Procedure

Mice were used as controls and blood recipients, and at 3- to 4-day intervals, 1 control mouse and 2 infected mice were necropsied, tissues were cultured, and a recipient mouse was inoculated with blood. Guinea pigs were randomized to 4 groups and inoculated intradermally with 100, 102, 103, or 104 spirochetes. For 48 days, clinical, hematologic, serologic, and microbiologic tests were performed on them, after which they were necropsied.

Results

In mice, spirochetemia was detectable between postinoculation days (PID) 3 and 13, and seroreactivity to homologous antigen was detectable during PID 10 through 31. Compared with control mice, infected mouse spleens were 2 to 3 times larger. Histologic lesions included lymphoid hyperplasia, neutrophilic panniculitis, epicarditis, and myocarditis, with intralesional spirochetes detected from PID 3 through 6. During PID 10 through 31, nonsuppurative epicarditis developed. Signs of illness and hematologic abnormalities were not observed in guinea pigs, despite isolating spirochetes from blood during PID 7 to 27. When necropsied on PID 48, histologic lesions included lymphoid hyperplasia and lymphocytic plasmacytic epicarditis.

Conclusions

The FCB isolate causes spirochetemia, lymphoid hyperplasia, dermatitis, and myocardial injury in Swiss Webster mice and can be transmitted by blood inoculation. In Hartley guinea pigs, the isolate causes spirochetemia, lymphoid hyperplasia, and epicarditis. Documentation of disease in mice, guinea pigs, and, presumably, dogs raises the level of concern that the FCB isolate might be pathogenic for man and other animal species. (Am J Vet Res 1996;57:505–511)

Free access
in American Journal of Veterinary Research

Abstract

Objectives

To determine whether the vaccine Brucella abortus strain RB51 (SRB51) would infect dogs, be shed in urine or feces, or cause placentitis and abortion.

Animals

18 Beagles.

Procedure

Males (n = 3), nonpregnant females (n = 3), and pregnant females (n = 4) were inoculated orally with SRB51; control dogs (n = 2) were fed sterile saline solution. A separate group of pregnant females (n = 5) received SRB51 IV, and their controls (n = 1) received sterile saline solution IV. Dogs were observed twice daily for evidence of abortion. Urine and feces were collected periodically for bacteriologic culture, and blood was collected for bacteriologic culture and serologic analysis. At full gestation (oral and IV inoculated pregnant females) or on postinoculation day 49 (nonpregnant females and males), dogs were euthanatized and samples were collected for bacteriologic culture and microscopic examination.

Results

Abortion was not apparent during the study, and SRB51 was not found in samples of urine or feces from any dog. Strain RB51 was isolated from retropharyngeal lymph nodes from all orally inoculated dogs (9/9). One orally inoculated and 1 IV inoculated pregnant dog had SRB51 in placental tissues. Strain RB51 was also isolated from 1 fetus from the orally inoculated female dog with placentitis, but lesions were not detected in the fetus.

Conclusions and Clinical Relevance

Oral inoculation of nonpregnant female or male dogs with SRB51 did not result in shedding in urine or feces, although oropharyngeal lymph nodes became infected; in pregnant females, it caused infection of the placenta, with resulting placentitis and fetal infection, but abortion was not apparent. Intravenous inoculation resulted in infection of maternal spleen, liver, and placenta; however, fetal infection and abortion were not observed. Infected canine placental membranes or fluids may be a source of infection for other animals and human beings. (Am J Vet Res 1997;58:851–856)

Free access
in American Journal of Veterinary Research