The role of T-lymphocytes in neuropathic pain initiation, development of chronicity and treatment.

Ongoing research has strongly suggested the role the immune system plays in the pathogenesis of neuropathic pain. T cells appear to be one of the main regulators of the immune system with many mediators appearing to promote or suppress pain resolution. Limited effective therapies are available for treatment of neuropathic pain. Treatments available appear to modulate specific T cell with altered ratios present 3 months post treatment and parallels clinical improvement. This further supports the neuro-immune basis for neuropathic pain chronicity. Identification of novel immune mediators involved in pain development may suggest new target areas in treatment.

Sequence variation at a Bmy I/Rsa I restriction site in ovine herpes virus 2.

DNA samples extracted from a bovine brain, one blood and one buffy coat sample from three cattle with malignant catarrhal fever, and from 47 samples of pooled sheep sera, were amplified by nested polymerase chain reaction (PCR) using primers specific for ovine herpes virus 2 (OHV-2). Confirmation of the specificity of the amplified DNA segment by restriction enzyme analysis with Rsa I and Bmy I as described by Baxter et al. was obtained in most samples. Nine amplified DNA samples could not be digested, or were only partially cut, with these enzymes. Sequencing of six samples revealed a two-nucleotide substitution in the middle of the restriction site (AA vs. CG) in four of these samples (the bovine brain and three sera), and two peaks at each of these positions (C or A, G or A) in two samples from pooled ovine serum. These results indicate the existence of a variant of OHV-2, and that both the previously sequenced OHV-2 and the variant were present in some samples of pooled ovine serum.

Eradication of ovine footrot by repeated daily footbathing in a solution of zinc sulphate with surfactant.

OBJECTIVE: To investigate the effect on ovine footrot of repeated daily footbathing in a solution of zinc sulphate with surfactant. DESIGN: Merino sheep were allocated to control and treatment groups of 119 sheep each at week 0. The sheep had a history of S1, U1, T and/or U6 types of Dichelobacter nodosus in interdigital and underrunning footrot lesions. Feet were not pared prior to treatment. PROCEDURE: Treatment sheep were footbathed in a 15 to 18% (w/v) solution of zinc sulphate with surfactant for 10 min on five consecutive days during week 1. At week 2, and fortnightly to week 52, all feet were inspected, lesion scores were recorded and samples were taken for laboratory tests. At week 53, all feet with no lesions at week 52, but with underrunning lesions prior to week 1, were pared and samples were taken. RESULTS: After footbathing, there were no lesions in any treatment sheep at any inspection to week 52. The percentage of feet of control sheep with lesions increased from 9% (391 of 4,284) between weeks 20 and 36, to 14% (593 of 4,284) between weeks 36 and 52. Ninety-five of 96 control sheep with no lesions at week 20 were still asymptomatic at week 52. D nodosus was not isolated from samples taken from 99 and 87 pared feet of treatment and control sheep, respectively. CONCLUSION: Repeated daily footbathing combined with prolonged exposure to a dry environment eradicated footrot in sheep with both interdigital and underrunning lesions in feet that were not pared prior to treatment.

Occurrence of different strains of Dichelobacter nodosus in new clinical lesions in sheep exposed to footrot associated with multi-strain infections.

OBJECTIVE: To investigate the occurrence of S1, U1 and T strains of Dichelobacter nodosus in new clinical lesions in sheep exposed to footrot associated with multi-strain infections. DESIGN: Seventy-seven donor sheep were grazed with 84 recipients for 33 weeks. The donor sheep were Merinos with a history of clinically virulent footrot associated with protease type S1, U1 and T strains of D nodosus that hybridised with gene sequences pJIR314B, pJIR318 and/or pB645-335. The recipient sheep were Merinos with no history of footrot. PROCEDURE: Each fortnight, all feet were examined, their lesion scores were recorded and samples of lesion material were taken for laboratory tests. RESULTS: Eighty-nine percent (299 of 336) of feet of recipient sheep developed new clinical lesions. S1, U1 and T strains of D nodosus were recovered from 58%, 22% and 18%, respectively, of these lesions at a ratio that remained constant during two apparent peaks in footrot transmission. Gene sequences homologous to pJIR314B and pB645-335 were detected in 56% (93 of 166) and 29% (48 of 166), respectively, of S1 strains of D nodosus at a ratio that was not constant during the experiment. CONCLUSIONS: S1 was the dominant protease type of D nodosus in new clinical lesions. The occurrence of S1 strains did not increase relative to U1 and T strains of D nodosus during the experiment. S1, U1 and T strains of D nodosus remained in equilibrium despite changes in environment, genetic types in the population of S1 strains, and host resistance to footrot.