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Biomedical subjects

J S Patterson

Publications and source records attributed to J S Patterson.

At least 19 recordsLinked to original sources

Preemptive intrathecal ketamine delays mechanical hyperalgesia in the neuropathic rat.

UNLABELLED: We studied the effect of preemptive intrathecal ketamine administration on the development of mechanical hyperalgesia in a rat model of mononeuropathy. Rats given intrathecal ketamine 1 mg/kg or normal saline were subsequently rendered neuropathic by placing four loose ligatures around the sciatic nerve. The onset of resultant hyperalgesia was evaluated using von Frey monofilaments. Preemptive ketamine significantly slowed the onset of mechanical hyperalgesia at both 2.35 g (P < 0.04) and 4.19 g (P < 0.05) thresholds through the third postoperative day but did not alter the ultimate degree of hyperalgesia in either severity or frequency in this model. We conclude that ketamine delayed the onset, but failed to prevent the development of, mechanical hyperalgesia in a rat model of peripheral mononeuropathy. IMPLICATIONS: Pain in response to light touch may follow nerve injury. Prevention of this complication would be clinically useful. Ketamine, an anesthetic, was administered spinally to rats before nerve injury in an attempt to prevent the development of chronic pain. Hypersensitivity to light touch was delayed by preemptive ketamine.

Anesthetics, Dissociative

Actinomycotic splenitis and intestinal volvulus in an alpaca (Lama pacos).

Morphologic, microbiologic, and polymerase chain reaction amplification techniques were used to evaluate an alpaca (Lama pacos) with splenitis and intestinal volvulus. The intestinal volvulus produced a severe necrosuppurative typhlocolitis associated with vascular thrombosis and was most likely the cause of death of this animal. In addition, this animal had multiple coalescing abscesses affecting most of the splenic tissue. The isolation of Actinomyces spp. from the spleen and the morphology of the colonies when stained with Gram and Steiner stains support a diagnosis of splenic actinomycosis.

Abscess

Protective effect of hypothermia and left heart bypass on spinal ischemia in the dog.

OBJECTIVE: To test the hypothesis that systemic hypothermia (SH) to 30 degrees C in combination with partial left heart bypass (PLHB) at either a high or low distal arterial perfusion pressure (DAPP) following 45 minutes of cross-clamp (XC) occlusion of the thoracic aorta will protect against clinical and histological spinal cord ischemia in the dog. DESIGN: A blinded, prospective, randomized, and controlled experimental trial. SETTING: Tertiary care center animal laboratory. PARTICIPANTS: Seventeen adult mongrel dogs. INTERVENTIONS: The animals were randomized into 5 groups: control group 1: XC plus no protection (n = 3); control group 2; XC plus systemic normothermia plus PLHB, with a DAPP less than 20 mm Hg (n = 3); treatment group 1: XC plus systemic normothermia plus PLHB, with a DAPP greater than 20 mm Hg (n = 3); treatment group 2: XC plus SH plus PLHB, with a DAPP greater than 20 mm Hg (n = 3); treatment group 3: XC plus SH plus PLHB, with a DAPP less than 20 mm Hg (n = 5). MAIN OUTCOME MEASURES: Clinical and histological neurological injury evaluation by separate blinded observers. RESULTS: Control animals were neurologically and histologically ischemic. Treatment animals were neurologically and histologically normal. Partial left heart bypass with a DAPP greater than 20 mm Hg prevented paraplegia, with either systemic normothermia or SH. Systemic hypothermia plus PLHB, even with a DAPP less than 20 mm Hg, protected against spinal cord ischemia during thoracic aortic occlusion. CONCLUSION: Systemic hypothermia to 30 degrees C combined with PLHB at either a high or low DAPP prevented spinal cord ischemia following thoracic aortic XC occlusion in our canine model and merits clinical trial in patients.

Animals

Sarcocystosis in mink (Mustela vison).

This report describes the clinical, microscopic, and ultrastructural findings in mink with muscular sarcocystosis. Three 2-3-mo-old mink were killed because they were ill with signs of progressive neurological disease. One mink had variable numbers of sarcocysts in multiple skeletal muscles. Sarcocysts were up to 300 microm in long and 20 microm wide. Ultrastructurally, the sarcocyst wall had numerous elongated 1.7-2.0-microm x 250-nm villar protrusions (VP). The VP had microtubules and irregularly distanced minute undulations. Both metrocytes and bradyzoites were present in sarcocysts. The mink with sarcocysts in muscles also had nonsuppurative meningoencephalitis and meningomyelitis. Similar brain lesions were found in other 2 mink from the same farm, but sarcocysts were not observed in the skeletal muscle of these animals. This is the first report of muscular sarcocystosis in mink.

Animals

Immunohistochemical diagnosis of eastern equine encephalomyelitis.

An immunohistochemical (IHC) assay was developed for the detection of eastern equine encephalomyelitis (EEE) virus antigen in formalin-fixed, paraffin-embedded tissues. All cases of EEE diagnosed at the Michigan State University Animal Health Diagnostic Laboratory from 1991 through 1994 were evaluated. The diagnosis was based on histopathologic examination of the brain and confirmatory virus, isolation. Sections of cerebrum from 26 equids and 5 birds were assessed by IHC. Histologically normal brain tissues from 2 horses and 1 pheasant and brain tissues from 2 cases of equine neurologic disease with diagnoses other than EEE served as negative controls. The IHC assay was based on standard streptavidin-biotin technology, using a commercially available kit and a monospecific polyclonal primary antibody preparation derived from murine ascitic fluid. Nineteen of 20 equids and all 5 birds positive by histopathology and virus isolation were positive for EEE virus antigen by IHC. Three equids with histologic lesions compatible with a diagnosis of EEE but negative by virus isolation also were negative for virus antigen by IHC. In 3 other equids, histopathology and IHC were positive for EEE, but virus isolation was not attempted because of contamination of the brain specimen. The IHC assay of formalin-fixed, paraffin-embedded brain tissues for EEE virus antigen is a rapid, effective test for confirming a histopathologic diagnosis of EEE, and assay results correlate well with virus isolation results.

Animals

Effect of the neodymium:yttrium aluminum garnet laser on postoperative neuroma formation after neurectomy in rats.

The effect of neodymium:yttrium aluminum garnet (Nd:YAG) laser-performed neurectomy was compared with conventional scalpel-performed neurectomy, using the rat sciatic nerve model. Sixteen male Sprague-Dawley rats underwent unilateral transection of the sciatic nerve by 1 of 3 methods. The sciatic nerve of rats under general anesthesia was transected by use of a steel scalpel blade (group 1, n = 5); a contact Nd:YAG laser at 6W of power (group 2, n = 6); or an Nd:YAG laser at 12 W of power (group 3, n = 5). Thirty days after surgery, all rats were euthanatized and the nerves were harvested, imbedded in paraffin, fixed, and sectioned for light microscopy. Neurodegenerative changes and perineurial cell proliferation were least severe in the nerves transected by use of a steel scalpel (group 1), and were most severe in nerves transected by use of laser at 6 W of power (group 2). There was a significant difference in prevalence of perineurial proliferation between the scalpel and laser neurectomy groups (P = 0.029). There was no significant difference in prevalence of neuroma formation or neurodegeneration between the laser and scalpel neurectomy groups, although neuromas were found in 3 rats (2 from group 2 and 1 from group 3). Within the limits of this study, we found that the Nd:YAG laser was less successful than sharp division, using a scalpel, in preventing neuroma formation after nerve transection.

Animals

Identification of opossums (Didelphis virginiana) as the putative definitive host of Sarcocystis neurona.

Sarcocystis neurona is an apicomplexan that causes equine protozoal myeloencephalitis (EPM) in North and South America. Horses appear to be an aberrant host, because the merozoites continually divide in the central nervous system, without encysting. The natural host species has not previously been identified. The small subunit ribosomal RNA (SSURNA) gene of S. neurona was compared to those of Sarcocystis muris, Sarcocystis cruzi, Toxoplasma gondii, and Cryptosporidium parvum to identify a unique region suitable for a species-specific amplification primer. The S. neurona SSURNA primer was used in a polymerase chain reaction (PCR) assay for the purpose of identifying this organism in feces and intestinal digest of wildlife specimens. Sporocysts were isolated from 4 raccoons (Procyon lotor), 2 opossums (Didelphis virginiana), 7 skunks (Mephitis mephitis), 6 cats (Felis catus), 1 hawk (Accipiter sp.), and 1 coyote (Canis latrans). The S. neurona SSURNA PCR assay and a control PCR assay using protist-specific primers were applied to all sporocyst DNA samples. All sporocyst DNA samples tested positive on the control assay. The SSURNA PCR assay yielded a 484-bp product only when applied to opossum samples. The SSURNA gene of both opossum sporocyst samples was sequenced to determine its relationship to the S. neurona SSURNA gene. The sequence had 99.89% similarity with S. neurona. This suggests that opossums are the definitive host of S. neurona.

Animals

Histologic and ultrastructural changes after large-colon torsion, with and without use of a specific platelet-activating factor antagonist (WEB 2086), in ponies.

The role of platelet-activating factor (PAF) in mediating the colonic damage that develops after large-colon torsion was studied in 14 ponies. Morphologic changes in areas of the ascending colon and selected abdominal and thoracic viscera after 1 hour of large-colon torsion and 3 to 5 hours of reperfusion were determined, as well as the protective effects of systemic administration of a specific PAF antagonist (WEB 2086). Ponies were selected then allocated at random and in equal numbers to 2 groups that received 1 of 2 treatments prior to induction of large-colon torsion: group 1--control (saline solution), and group 2--WEB 2086 (3 mg/kg of body weight loading dose and 3 mg/kg/h for the remainder of the study). In each pony, full-thickness tissue specimens from the gastrointestinal tract--cecum, pelvic flexure, left and right ventral colon, and right dorsal colon--heart, left lung, liver, left adrenal gland, spleen, and right kidney were collected and histologically evaluated. Edema, mucosal necrosis, and neutrophil infiltration in colonic sections were graded from 0 (normal) to 3 (most severe changes). Sections of liver and lung from 3 ponies in each group, and colon from 1 pony in each group, also were examined by transmission electron microscopy to determine the presence of ultrastructural alterations. Ischemia and reperfusion induced marked changes in all sections of colon in all ponies: moderate to severe submucosal edema, moderate necrosis of the superficial epithelium and lamina propria, and necrosis of the mucosal crypt epithelium. Extravascular neutrophil accumulation was evident in all sections of colon and cecum, but not in other tissues.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals

Investigation of an epizootic of bovine viral diarrhea virus infection in calves.

Eight of 19 calves born to bovine viral diarrhea virus (BVDV)-negative and -immunocompetent dams were determined to be infected with a noncytopathic strain of BVDV. Six of the 8 calves had diarrhea and 2 had no clinical signs of disease. In 3 euthanatized calves, lesions consistent with mucosal disease were found throughout the gastrointestinal tract, and the virus was isolated from the spleen, lymph nodes, and small intestine. In 5 calves, BVDV was isolated from mononuclear cells in blood samples obtained 21 days apart, indicating persistent infection. The virus was not isolated from sera obtained from 2 calves, with chronic nonclinical infections, that had neutralizing antibody titers > or = 1:512 against bovine viral diarrhea-Singer virus and titers > or = 1:256 against the persistent BVDV. Twenty-one days after vaccination with a vaccine that contained inactivated noncytopathic and cytopathic biotypes of BVDV, 4 of 5 persistently infected calves had neutralizing antibody titers < or = 1:4 against the bovine viral diarrhea-Singer virus and their persistent virus. Prior to vaccination, 2 of 11 virus-negative calves had neutralizing antibody titers < or = 1:128 against the bovine viral diarrhea-Singer virus, and after vaccination, only 1 virus-negative calf had a titer < or = 1:512. At 149 days after revaccination and prior to weaning, 4 virus-negative calves had neutralizing antibody titers < or = 1:512 (range, 1:16 to 1:384). Under the specific conditions in this herd, we were not able to detect a beneficial effect of vaccination.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals

A longitudinal study of rotavirus antibody titers in swine in a closed specific pathogen-free herd.

In a newly established closed specific pathogen-free (SPF) swine herd, gilt/sow suckling and weaned pig rotavirus specific antibody titers were followed for three lactations by enzyme-linked immunosorbent assay (ELISA) to gain insight into the dynamics of herd antibody titers to group A rotavirus. Among gilts/sows, serum antirotavirus IgG titers increased during each lactation with a subsequent drop in titer between farrowings. Serum antirotavirus IgM titers declined during each lactation and with subsequent parity. Serum antirotavirus IgA titers remained constant during lactations and among parities. In colostrum and milk, antirotavirus IgA antibody was abundant. Differences in titer were not noticed between gilts and second litter sows but third litter sows had significantly higher titers than the first two groups. Antirotavirus IgG was high in colostrum but nearly nonexistent in milk. This titer did not vary significantly within or among parities. There was a linear regression in the titers of baby pig serum antirotavirus IgG from the post colostral sample through to seven weeks old, after which titer began to increase. No difference in baby pig serum antirotavirus IgG was noted among the three litters. Serum antirotavirus IgA and IgM were undetectable in baby pig sera after 2-3 weeks of age. Coproantibody to rotavirus was sporadically present in pig feces for 2-3 weeks after birth with highest titers in the IgA fraction. We conclude that although it is probable that age resistance of pigs to rotavirus diarrhea occurs, humoral immunity as measured by ELISA rotavirus antibody titers may not be intimately involved in virus clearance since in our studies baby pigs passively received large amounts of antibody but still excreted pathogenic virus. The finding of increasing levels of serum antirotavirus IgG in gilt/sow serum suggest that exposure to antigen of dams occur without significant increases in antirotavirus IgG titers in either colostrum, milk, or baby pig serum.

Animals

The role of passive immunity in bovine respiratory syncytial virus-infected calves.

The role of passive immunity in bovine respiratory syncytial virus (BRSV) infections in neonatal calves was evaluated. Calves were divided into groups as follows: colostrum-deprived, sham-inoculated; colostrum-deprived, BRSV-inoculated; and colostrum-fed, BRSV-inoculated. Calves were inoculated with a low-passage field isolate of BRSV for 4 consecutive days by a combined respiratory tract route and were euthanized 6 days after receiving the last inoculation. Arterial oxygen tension (Pao2) decreased significantly over time in colostrum-deprived, BRSV-inoculated calves (P less than .01) and was significantly different among treatment groups (P less than .05). A significant decrease in arterial oxygen saturation was observed in this same group over time (P less than .01). Mean percentage of pneumonic lung volume (determined by computer data digitalization) was significantly greater in infected, colostrum-deprived calves compared with the other groups (P less than .01), and BRSV antigen was detected in these calves by avidin-biotin immunoperoxidase staining. Thus, passive immunity derived from colostrum feeding decreased the severity of BRSV infections in calves.

Analysis of Variance

Neuropathology of bovine beta-mannosidosis.

beta-Mannosidosis, an inherited defect of glycoprotein catabolism previously identified in goats and humans, has been recently diagnosed in Salers cattle. This disorder is associated with deficiency of lysosomal beta-mannosidase and accumulation of oligosaccharides. Analysis of bovine beta-mannosidosis neuropathology was initiated to determine whether independently arising gene defects in cattle and goats result in expression of similar lesions. Brain, spinal cord, and selected peripheral nerves from seven affected newborn Salers calves and three normal newborn calves were available for gross, light microscopic, and electron microscopic analysis. Gross examination revealed hydrocephalus of variable severity and myelin deficiency in the cerebral hemispheres, cerebellum, and brainstem. Microscopic examination revealed cytoplasmic vacuolation, myelin deficiency, and axonal spheroids of similar type and distribution to that reported in affected goats. Cytoplasmic vacuolation resulting from lysosomal storage showed consistent variation among cell types. Myelin deficits were more severe in the cerebral hemispheres and cerebellum than in the spinal cord. Axonal spheroids occurred in the cerebrum, brainstem, cerebellum, and trigeminal nerve endings. The presence of similar lesions in bovine and caprine beta-mannosidosis supports a direct relationship with the gene defect.

Animals