Because articular chondrocytes are a target for drugs that can influence the integrity of cartilage, we investigated the effects of 3 antiarthritic drugs, glycosaminoglycan polysulfate, diclofenac-Na, and S-adenosylmethionine sulfate p-toluenesulfonate on total protein, fibronectin, and DNA synthesis, as well as on extradomain-A fibronectin and keratan sulfate content. Glycosaminoglycan polysulfate stimulated dose-dependent incorporation of [35S]methionine into protein and fibronectin, whereas incorporation of [3H]thymidine into DNA was unaffected. Total fibronectin, extradomain-A fibronectin, and keratan sulfate content were high in chondrocyte cultures treated with glycosaminoglycan polysulfate. In contrast, fibronectin and DNA synthesis, as well as extradomain-A fibronectin and keratan sulfate content were unaffected by diclofenac-Na. S-adenosylmethionine decreased dose-dependently the synthesis of fibronectin, as well as the content of fibronectin and keratan sulfate. At the highest concentration of S-adenosylmethionine tested, findings suggest that cell viability was impaired as assessed by the release of lactate dehydrogenase into the media.

High molecular weight (MW) hyaluronate (HA) is an integral part of synovial fluid (SF), regulating many important physiologic and pathophysiologic mechanisms. Many of its effects depend on, or are reflected in, the concentration and MW of HA. High-performance liquid chromatography was used to assess simultaneously the concentration and MW of HA in SF obtained from horses with various arthritides: acute traumatic arthritis; chronic traumatic arthritis, including degenerative joint disease (DJD); and infectious arthritis. The size-exclusion column was calibrated, using appropriate HA concentration and MW standards, before the high-performance liquid chromatographic assays of the SF samples. Calibration of the column disclosed that the maximal limit for MW estimation of HA was around 3 million. In control joints, MW of HA ranged from 2 to 3 X 10(6) (mean 2.5 X 10(6)) and did not differ significantly from MW of HA in SF from horses with acute or chronic traumatic arthritis (mean 2 x 10(6); range 1.5 to 3 x 10(6)). Interestingly, a small amount of HA of moderately high MW (approx 1 to 1.5 x 10(6)) was detected in chromatograms of SF from infected joints. This degree of polymerization of SF HA was significantly (P < 0.01) lower, compared with that for control joints. There was no difference in mean (+/- SD) concentration of HA between control joints and joints with acute or chronic traumatic arthritis (0.33 +/- 0.12 g/L vs 0.18 +/- 0.03 g/L or 0.23 +/- 0.12 g/L), indicating that SF HA concentration probably should not be used as a diagnostic marker for the condition. However, the SF HA concentration was significantly (P < 0.01) lower in joints with infectious arthritis (0.07 +/- 0.03 g/L) and in the joints with radiographic evidence of DJD (0.12 +/- 0.01 g/L), compared with control joints.

The nature of Mycoplasma arthritidis antigens responsible for eliciting protective immunity in rats was studied by inoculation of rats with mycoplasmal components that had been subjected to a variety of physical and chemical treatments. All inocula tested induced good protection against development of clinical illness, as assessed by changes in body weight and appearance of joint swelling and/or temporary hind limb paralysis. Although all preparations stimulated development in inoculated rats of high titer of antimycoplasmal antibodies measured by ELISA, the complement-fixation antibody response was poor and, in some cases, lacking altogether. This indicated that completion-fixation antibodies may not be involved in protecting rats against M arthritidis-induced illness. Protective antigens were stable to heat (100 C for 10 minutes), formalin, and denaturation by sodium dodecyl sulfate (SDS). Inoculation with membrane and soluble cytoplasmic fractions was protective, as was inoculation with 5 M arthritidis fractions separated according to molecular weight by SDS-polyacrylamide gel electrophoresis (SDS-PAGE). For this latter experiment, rat antisera obtained after vaccination, but prior to challenge exposure, were tested by immunoblot analysis against electrophoretically separated M arthritidis membrane proteins. Interestingly, all antisera from these rats recognized antigens migrating far outside the molecular weight range of the cell fractions with which rats were inoculated. This indicated either that the protective antigens may be composed of numerous antigenically related subunits that separated by SDS-PAGE into a variety of molecular weight ranges or that a few major antigens may exist in several forms or phases within a given population of M arthritidis.

The effect of pulsed radio frequency therapy (PRFT) was evaluated on seven ponies with no arthritis and in 28 ponies in which arthritis was created using intra-articular amphotericin B to induce synovitis in the right middle carpal joint. The ponies were divided into five treatment and two control groups. Two levels of arthritis were created and two dosage levels of PRFT were evaluated. The effect of PRFT on arthritic and nonarthritic joints was measured by comparing synovial fluid parameters, the degree and duration of lameness, the range of carpal motion, and carpus circumference, for treated and untreated groups. Lesions seen radiographically at gross pathology, and by histopathology were also compared between the treated and control groups. In the ponies with a mild form of induced arthritis, PRFT significantly (p < 0.05) reduced the severity and duration of lameness, swelling of the carpus, and the severity of gross pathological and radiographic changes. In these ponies the synovial acid phosphatase levels were lower, the mucin clot quality was superior, and the synovial protein levels were lower for the ponies receiving PRFT as compared to the arthritic ponies receiving no treatment. A dose response effect was evident. In ponies with a slightly more severe form of arthritis, PRFT was evaluated at one dosage level. The treated ponies were significantly improved over the untreated ponies with respect to carpal range of motion, degree of lameness, carpus swelling, and radiographic lesions. No deleterious effects were noted when normal, PRFT treated, middle carpal joints were compared to contralateral untreated, normal joints. It was concluded that significant beneficial effects resulted when affected ponies were treated with PRFT.

Log-linear methodology was used to examine relations among caprine arthritis-encephalitis virus (CAEV) seroreactivity and host/management factors in a cross-sectional study of 2,826 goats on 13 California dairies. The CAEV serologic status was associated with age and feeding method (pasteurized/unpasteurized milk), but not with breed. Data from a prevalence survey of 321 goats from 2 additional dairies demonstrated very good fit of the selected log-linear model (P = 1.00), indicating that the model was very appropriate to describe the relations. Odds of seropositivity and odds ratios were generated by use of a logit model derived from the log-linear model. Goats raised by the unpasteurized feeding method were estimated to have been 3.3 times more likely to be CAEV-seropositive than goats fed by the pasteurized method, when adjusted for the effects of age. Goats aged 2, 3, 4, and 5 or greater years were estimated to have been 1.7, 2.6, 4.5, and 5.7 times, respectively, more likely to be CAEV-seropositive than were yearling goats when ratios were adjusted for pasteurization status. Breed, gender, and herd of origin were not associated with CAEV seroreactivity when the effects of other factors were considered. Estimated odds of CAEV seroreactivity and the associated odds ratios for combinations of factor levels are reported. In this study, the magnitude and direction of the associations among CAEV serologic status, age, and pasteurized feeding methods were demonstrated.

Polysulfated glycosaminoglycan (PSGAG) recently have been reported to potentiate the infectivity of Staphylococcus aureus in horses with experimentally induced septic arthritis. Four groups of 8 horses each had 1 midcarpal joint injected with approximately 33 viable colony-forming units (CFU) of S aureus plus either 1 ml of saline solution (group 1), 250 mg of PSGAG (group 2), 250 mg of PSGAG passed through a 0.6-micrometer filter (group 3), or 250 mg of PSGAG plus 125 mg of amikacin (group 4). Horses that developed clinical signs consistent with sepsis were euthanatized, and samples were collected at necropsy. Horses that survived had samples obtained by use of arthroscopy at days 13 and 14 after injection. Staphylococcus aureus was isolated from 1 group-1 horse, 8 group-2 horses, and 7 of 7 group-3 horses that met protocol, but was not isolated from any group-4 horses. All 16 aforementioned horses had clinical signs, results of synovial fluid analysis, and gross pathologic and synovial membrane histopathologic findings that were consistent with septic arthritis. Polysulfated glycosaminoglycan (250 mg) increased the infectivity of 33 CFU of S aureus (P = 0.001); filtering the PSGAG had no effect. Intra-articular injection of 125 mg of amikacin immediately after inoculating the joint with 33 CFU of S aureus significantly (P = 0.001) decreased potentiation of infection by the PSGAG.

Adult Beagles were used to evaluate clinical signs and serologic response after inoculation with, or exposure to, Borrelia burgdorferi. An indirect immunofluorescent assay (IFA) and 2 ELISA were used to monitor the serologic response to B burgdorferi. Feeding infected ticks on 4 dogs (group 1) failed to cause seroconversion, and SC inoculation with 500 organisms caused minimal seroconversion in 2 of 4 dogs (group 2). At 56 days, approximately 3.01 X 10(8) B burgdorferi organisms were injected IV into group-1 dogs, and intraperitoneally into group-2 dogs. A control group of 4 dogs (group 3) had noninfected ticks feed on them, and then were given IV injection of physiologic saline solution. Increases in immunoglobulin M (IgM) titers were detected in 2 of 4 group-2 dogs approximately 7 days after the initial exposure. These titers returned to negligible values 20 days later. Immunoglobulin G titers increased approximately 10 days after the initial exposure and were mildly increased 56 days later, when dogs were exposed a second time. Both the IV and intraperitoneal injections (second exposures) resulted in increased IgM titers, which in both groups eventually returned to preexposure values after approximately 2 months. Immunoglobulin G titers increased within a week after the second exposure, and in 3 dogs monitored for 8 months, returned to negligible values after the 8-month period. One control dog had a slightly increased IgG titer 24 days after the second inoculation. The possibility of urine transmission is suggested. Clinical status, hemograms, serum biochemical profiles, ECG and results of urinalyses remained normal throughout the study. Borrelia burgdorferi was not isolated from either the blood or urine of these dogs. Gross or microscopic pathologic changes were not detected on necropsy.