A challenge-exposure model was developed for dose-dependent induction of subclinical (moderate) atrophic rhinitis (AR) in conventionally raised Dutch Landrace and Large White pigs, about 4 weeks old. Under favorable climatic and housing conditions, pigs were intranasally challenge-exposed with Pasteurella multocida-derived toxin (Pm-T) 3 days after pretreatment by inoculation with 1% acetic acid. Pigs were challenge-exposed with 1 of the following Pm-T doses: 0 (control), 5, 13, 20, or 40 microgram of Pm-T/ml of phosphate-buffered saline solution (PBSS), 0.5 ml/ nostril/d on 3 consecutive days. Five weeks after challenge exposure, subclinical moderate) AR status was defined as intermediate conchal atrophy (grade 2 for ventral conchae on a 0 to 4 scale and grade 1 or 2 for dorsal conchae on a 0 to 3 scale, respectively) and perceptible difference in change in brachygnathia superior (CBS) between control and challenge-exposed pigs between the beginning and end of the study. All Pm-T-exposed pigs had nasal damage that was dose-dependent. The higher Pm-T doses resulted in higher ventral conchae atrophy and dorsal conchae atrophy scores. The CBS increased with applied Pm-T dose, resulting in significant (P < 0.05) differences between controls (3.88 mm) and the 13-, 20-, and 40-microgram Pm-T-treated groups (7.77, 6.58, and 7.98 mm, respectively). In response to the applied dose, weight gain per week for Pm-T-exposed pigs was lower than that of controls after week 3 (P < 0.01). Difference from controls was 32, 54, 52, and 96 g/d/pig for 5-, 13-, 20-, and 40-microgram Pm-T-treated groups respectively, in the last 2 weeks. For Dutch Landrace and Large White pigs, intranasally administered Pm-T mimicked the pathogenic effect of in vivo infection with toxigenic Pm strains. The optimal model to induce subclinical AR appeared to be 13 microgram of Pm-T/ml (0.5 ml/nostril/d) on 3 consecutive days. Our model should enable studies of exogenous and endogenous factors involved in development of AR, independent of the colonizing ability of the Pm strain used.

A challenge-exposure model was developed for dose-dependent induction of subclinical (moderate) atrophic rhinitis (AR) in conventionally raised Dutch Landrace and Large White pigs, about 4 weeks old. Under favorable climatic and housing conditions, pigs were intranasally challenge-exposed with Pasteurella multocida-derived toxin (Pm-T) 3 days after pretreatment by inoculation with 1% acetic acid. Pigs were challenge-exposed with 1 of the following Pm-T doses: 0 (control), 5, 13, 20, or 40 microgram of Pm-T/ml of phosphate-buffered saline solution (PBSS), 0.5 ml/ nostril/d on 3 consecutive days. Five weeks after challenge exposure, subclinical moderate) AR status was defined as intermediate conchal atrophy (grade 2 for ventral conchae on a 0 to 4 scale and grade 1 or 2 for dorsal conchae on a 0 to 3 scale, respectively) and perceptible difference in change in brachygnathia superior (CBS) between control and challenge-exposed pigs between the beginning and end of the study. All Pm-T-exposed pigs had nasal damage that was dose-dependent. The higher Pm-T doses resulted in higher ventral conchae atrophy and dorsal conchae atrophy scores. The CBS increased with applied Pm-T dose, resulting in significant (P < 0.05) differences between controls (3.88 mm) and the 13-, 20-, and 40-microgram Pm-T-treated groups (7.77, 6.58, and 7.98 mm, respectively). In response to the applied dose, weight gain per week for Pm-T-exposed pigs was lower than that of controls after week 3 (P < 0.01). Difference from controls was 32, 54, 52, and 96 g/d/pig for 5-, 13-, 20-, and 40-microgram Pm-T-treated groups respectively, in the last 2 weeks. For Dutch Landrace and Large White pigs, intranasally administered Pm-T mimicked the pathogenic effect of in vivo infection with toxigenic Pm strains. The optimal model to induce subclinical AR appeared to be 13 microgram of Pm-T/ml (0.5 ml/nostril/d) on 3 consecutive days.

We evaluated the effectiveness of 2 dopamine antagonists as treatments for fescue toxicosis in horses. Sixteen gravid mares were assigned by breed and expected foaling date to 1 of 3 treatment groups: endophyte-infested control 1.1 mg of domperidone/kg of body weight/d; and 3.3 mg of sulpiride/kg/d. Mares were pastured on endophyte-infected fescue and received 0.454 kg of a corn and dried molasses carrier containing the drug treatment. Treatment started 30 days prior to expected foaling date and continued until parturition. Blood samples were collected, and mammary gland scores were recorded every 5 days. Body weight and body condition scores were obtained every 28 days. Serum was analyzed for prolactin, progesterone, and estradiol-17beta concentrations. Domperidone-treated mares had shorter (P = 0.09) gestation duration and foaled closer (P = 0.07) to their expected parturition date than did control mares. Mammary gland scores were higher (P < 0.05) for domperidone-treated mares than for control mares. By 4 and 9 days after the start of treatment, serum prolactin concentration was higher P < 0.05) in domperidone-treated mares and sulpiride-treated mares, respectively, than in control mares. Domperidone- and and sulpiride-treated mares had higher (P < 0.05) serum progesterone and lower (P < 0.01) estradiol-17beta concentrations than did control mares. These results indicate that domperidone may offer considerable potential as a treatment for fescue toxicosis in horses.

We evaluated the effectiveness of 2 dopamine antagonists as treatments for fescue toxicosis in horses. Sixteen gravid mares were assigned by breed and expected foaling date to 1 of 3 treatment groups: endophyte-infested control 1.1 mg of domperidone/kg of body weight/d; and 3.3 mg of sulpiride/kg/d. Mares were pastured on endophyte-infected fescue and received 0.454 kg of a corn and dried molasses carrier containing the drug treatment. Treatment started 30 days prior to expected foaling date and continued until parturition. Blood samples were collected, and mammary gland scores were recorded every 5 days. Body weight and body condition scores were obtained every 28 days. Serum was analyzed for prolactin, progesterone, and estradiol-17beta concentrations. Domperidone-treated mares had shorter (P = 0.09) gestation duration and foaled closer (P = 0.07) to their expected parturition date than did control mares. Mammary gland scores were higher (P < 0.05) for domperidone-treated mares than for control mares. By 4 and 9 days after the start of treatment, serum prolactin concentration was higher P < 0.05) in domperidone-treated mares and sulpiride-treated mares, respectively, than in control mares. Domperidone- and and sulpiride-treated mares had higher (P < 0.05) serum progesterone and lower (P < 0.01) estradiol-17beta concentrations than did control mares. These results indicate that domperidone may offer considerable potential as a treatment for fescue toxicosis in horses.

The efficacy of 4-methylpyrazole (4-MP) and ethanol as treatment for ethylene glycol (EG) intoxication in cats was compared. Twenty-two cats were assigned at random to 6 experimental groups. Cats of 1 experimental group were given only 4-MP; those of another experimental group were given only EG. Cats of 3 experimental groups were intoxicated with EG and given 4-MP at 0 hour or 2 or 3 hours after EG ingestion, and those of 1 experimental group were given EG and treated with ethanol 3 hours after EG ingestion. Physical, biochemical, hematologic, blood gas, serum and urine EG concentrations, and urinalysis findings were evaluated at 0, 1, 3, 6, 9, 12, 24, 48, and 72 hours, 1 week, and 2 weeks after EG ingestion, or 4-MP treatment in cats of the 4-MP only group. The half-life of EG and percentage of ingested EG excreted unchanged were determined for each group. 4-Methylpyrazole treatment at 0 hour was most effective at preventing metabolism of EG. 4-Methylpyrazole was not effective in preventing development of renal failure when given 2 or 3 hours after EG ingestion. Ethanol given 3 hours after EG ingestion was successful in preventing development of renal dysfunction in 2 of the 6 cats treated 3 hours after EG ingestion. Of the remaining 4 cats treated with ethanol, 2 developed transient renal dysfunction and 2 developed acute oliguric renal failure and were euthanatized. 4-Methylpyrazol given 2 or 3 hours after EG ingestion was less effective in preventing EG metabolism than was ethanol given 3 hours after EG ingestion. Therefore 4-MP, at the dose found to be effective in dogs, cannot be recommended as an alternative to ethanol for treatment of EG intoxication in cats.

The efficacy of 4-methylpyrazole (4-MP) and ethanol as treatment for ethylene glycol (EG) intoxication in cats was compared. Twenty-two cats were assigned at random to 6 experimental groups. Cats of 1 experimental group were given only 4-MP; those of another experimental group were given only EG. Cats of 3 experimental groups were intoxicated with EG and given 4-MP at 0 hour or 2 or 3 hours after EG ingestion, and those of 1 experimental group were given EG and treated with ethanol 3 hours after EG ingestion. Physical, biochemical, hematologic, blood gas, serum and urine EG concentrations, and urinalysis findings were evaluated at 0, 1, 3, 6, 9, 12, 24, 48, and 72 hours, 1 week, and 2 weeks after EG ingestion, or 4-MP treatment in cats of the 4-MP only group. The half-life of EG and percentage of ingested EG excreted unchanged were determined for each group. 4-Methylpyrazole treatment at 0 hour was most effective at preventing metabolism of EG. 4-Methylpyrazole was not effective in preventing development of renal failure when given 2 or 3 hours after EG ingestion. Ethanol given 3 hours after EG ingestion was successful in preventing development of renal dysfunction in 2 of the 6 cats treated 3 hours after EG ingestion. Of the remaining 4 cats treated with ethanol, 2 developed transient renal dysfunction and 2 developed acute oliguric renal failure and were euthanatized. 4-Methylpyrazol given 2 or 3 hours after EG ingestion was less effective in preventing EG metabolism than was ethanol given 3 hours after EG ingestion. Therefore 4-MP, at the dose found to be effective in dogs, cannot be recommended as an alternative to ethanol for treatment of EG intoxication in cats.

Staphylococcal antigens and immune complexes (IC) prepared from antigen and hyperimmune canine serum were tested for their effects on certain functions of mononuclear (MN) and polymorphonuclear (PMN) leukocytes (cells) obtained from healthy dogs. The effect on MN cells was studied by determining the ability of antigen or IC to augment or inhibit mitogenesis induced by phytohemagglutinin (PHA). The effect of antigen or IC on PHA cells was studied by measurement of H2O2 production as an indicator of respiratory burst. Neither the antigen nor the IC, when cultured with MN cells, was mitogenic. Coincubation of antigen or IC with MN cells and PHA resulted in a concentration-dependent decrease in mitogenesis. The decreased mitogenesis could not be overcome by addition of excess PHA, and may in part have been related to toxic effects of the antigen or IC on MN cells. When MN cells were instead preincubated with antigen or IC, then washed and stimulated with PHA, there was still a concentration-dependent inhibition of mitogenesis, although toxicity to the cells was not observed. Low concentrations of staphylococcal antigen or IC stimulated slight H2O2 production by PHA cells. When PHA cells were coincubated with IC and another stimulus (opsonized zymosan or phorbol myristate acetate), IC appeared to augment phorbol myristate acetate-, but not zymosan-induced stimulation. These results suggest that staphylococcal antigens, either alone or complexed with antibody, have the ability to stimulate PMN cells and inhibit MN cell function. Such actions may have a role in the pathogenesis of recurrent staphylococcal infection in canine patients.

Staphylococcal antigens and immune complexes (IC) prepared from antigen and hyperimmune canine serum were tested for their effects on certain functions of mononuclear (MN) and polymorphonuclear (PMN) leukocytes (cells) obtained from healthy dogs. The effect on MN cells was studied by determining the ability of antigen or IC to augment or inhibit mitogenesis induced by phytohemagglutinin (PHA). The effect of antigen or IC on PHA cells was studied by measurement of H2O2 production as an indicator of respiratory burst. Neither the antigen nor the IC, when cultured with MN cells, was mitogenic. Coincubation of antigen or IC with MN cells and PHA resulted in a concentration-dependent decrease in mitogenesis. The decreased mitogenesis could not be overcome by addition of excess PHA, and may in part have been related to toxic effects of the antigen or IC on MN cells. When MN cells were instead preincubated with antigen or IC, then washed and stimulated with PHA, there was still a concentration-dependent inhibition of mitogenesis, although toxicity to the cells was not observed. Low concentrations of staphylococcal antigen or IC stimulated slight H2O2 production by PHA cells. When PHA cells were coincubated with IC and another stimulus (opsonized zymosan or phorbol myristate acetate), IC appeared to augment phorbol myristate acetate-, but not zymosan-induced stimulation. These results suggest that staphylococcal antigens, either alone or complexed with antibody, have the ability to stimulate PMN cells and inhibit MN cell function. Such actions may have a role in the pathogenesis of recurrent staphylococcal infection in canine patients.

A relation exists between colloid osmotic pressure and serum total protein concentration; equations describing this relation have been used to determine a calculated value for colloid osmotic pressure. However, the relation between total protein concentration and colloid osmotic pressure is altered by the method used to measure protein and by changes in the ratio of concentrations of albumin (A) to globulin (G). We developed nomograms for estimating colloid osmotic pressure from A and G concentrations, using samples obtained from clinically normal animals and compared the accuracy of these nomograms with that of previously described equations relating colloid osmotic pressure to total protein concentration. For comparison, serum samples from canine (n = 106), equine (n = 79), feline (n = 24), and bovine (n = 27) patients admitted to the University of Georgia Veterinary Medical Teaching Hospital were used. Results indicated that nomograms based on protein concentration estimated by a refractometer generally were the least reliable. Although predictive nomograms, using total protein concentration determined by the biuret method, provided better results for serum samples, there was considerable variation between measured and calculated values for colloid osmotic pressure in all species studied. Calculated values for colloid osmotic pressure derived from A and G concentrations were most closely related to measured values for colloid osmotic pressure in dogs, horses, and cats. However, calculated values for colloid osmotic pressure differed from measured values by as much as 5 mm of Hg for some samples by each of the methods of estimation. These results indicate that, although calculated values for colloid osmotic pressure may be most accurate when variations in the A-to-G ratio are accounted for in the nomogram, none of the calculation methods provided a consistently accurate estimate of colloid osmotic pressure. For clinical patients, colloid osmotic pressure based on these nomograms cannot replace direct measurement.

A relation exists between colloid osmotic pressure and serum total protein concentration; equations describing this relation have been used to determine a calculated value for colloid osmotic pressure. However, the relation between total protein concentration and colloid osmotic pressure is altered by the method used to measure protein and by changes in the ratio of concentrations of albumin (A) to globulin (G). We developed nomograms for estimating colloid osmotic pressure from A and G concentrations, using samples obtained from clinically normal animals and compared the accuracy of these nomograms with that of previously described equations relating colloid osmotic pressure to total protein concentration. For comparison, serum samples from canine (n = 106), equine (n = 79), feline (n = 24), and bovine (n = 27) patients admitted to the University of Georgia Veterinary Medical Teaching Hospital were used. Results indicated that nomograms based on protein concentration estimated by a refractometer generally were the least reliable. Although predictive nomograms, using total protein concentration determined by the biuret method, provided better results for serum samples, there was considerable variation between measured and calculated values for colloid osmotic pressure in all species studied. Calculated values for colloid osmotic pressure derived from A and G concentrations were most closely related to measured values for colloid osmotic pressure in dogs, horses, and cats. However, calculated values for colloid osmotic pressure differed from measured values by as much as 5 mm of Hg for some samples by each of the methods of estimation. These results indicate that, although calculated values for colloid osmotic pressure may be most accurate when variations in the A-to-G ratio are accounted for in the nomogram, none of the calculation methods provided a consistently accurate estimate of colloid osmotic pressure.

Effect of estrogen (E2) and progesterone (P4) on uterine antibacterial activity and immunoglobulin concentrations in mares was studied. In 2 in vitro experiments, 6 mixed-breed mares were ovariectomized, and uterine fluid and blood serum were analyzed. Antibacterial assay methods were used to determine inhibitory effects on Streptococcus zooepidemicus of uterine fluid samples collected on days 3, 5, and 8, and serum obtained on day 8 of treatment. Single radial immunodiffusion methods were used to quantify amounts of IgA and IgG in uterine fluid and serum on days 3, 5, 8, and 14 of treatment. Neither E2 nor P4 increased activity of serum and uterine fluid against S zooepidemicus. Numbers of colony-forming units per milliliter of bacteria were significantly (P < 0.01) lower in control Hanks' balanced salt solution with 1.0% gelatin (HBSSG) than in uterine fluids. Bacterial numbers were significantly (50%) greater in uterine fluids and serum than in HBSSG controls for both treatments. Both fluids, especially serum, supported significantly (P < 0.01) more growth of S zooepidemicus than did HBSSG when incubated for 0, 2, and 4 hours. These findings are in contrast to previous reports of antibacterial activity in the uterus of sexually intact mares undergoing an estrous cycle: great reduction of bacterial count in uterine fluid from mares in diestrus, and significant increases in bacterial numbers in uterine fluid or serum from mares in estrus. Treatment comparisons between serum and uterine fluid IgA and IgG concentrations were not significantly different, although overall IgA concentration in the uterus was higher than concentration in serum. The IgG concentration in uterine fluid was higher in P4- than E2-treated mares. However, IgG concentration was significantly (P < 0.01) higher in uterine fluid on day 8 in P4-treated mares than on day 3 or 5. Results of this study indicate that neither immunoglobulin concentration nor hormone treatment has a direct effect on streptocidal activity.

Effect of estrogen (E2) and progesterone (P4) on uterine antibacterial activity and immunoglobulin concentrations in mares was studied. In 2 in vitro experiments, 6 mixed-breed mares were ovariectomized, and uterine fluid and blood serum were analyzed. Antibacterial assay methods were used to determine inhibitory effects on Streptococcus zooepidemicus of uterine fluid samples collected on days 3, 5, and 8, and serum obtained on day 8 of treatment. Single radial immunodiffusion methods were used to quantify amounts of IgA and IgG in uterine fluid and serum on days 3, 5, 8, and 14 of treatment. Neither E2 nor P4 increased activity of serum and uterine fluid against S zooepidemicus. Numbers of colony-forming units per milliliter of bacteria were significantly (P < 0.01) lower in control Hanks' balanced salt solution with 1.0% gelatin (HBSSG) than in uterine fluids. Bacterial numbers were significantly (50%) greater in uterine fluids and serum than in HBSSG controls for both treatments. Both fluids, especially serum, supported significantly (P < 0.01) more growth of S zooepidemicus than did HBSSG when incubated for 0, 2, and 4 hours. These findings are in contrast to previous reports of antibacterial activity in the uterus of sexually intact mares undergoing an estrous cycle: great reduction of bacterial count in uterine fluid from mares in diestrus, and significant increases in bacterial numbers in uterine fluid or serum from mares in estrus. Treatment comparisons between serum and uterine fluid IgA and IgG concentrations were not significantly different, although overall IgA concentration in the uterus was higher than concentration in serum. The IgG concentration in uterine fluid was higher in P4- than E2-treated mares. However, IgG concentration was significantly (P < 0.01) higher in uterine fluid on day 8 in P4-treated mares than on day 3 or 5. Results of this study indicate that neither immunoglobulin concentration nor hormone treatment has a direct effec.

Serum C-reactive protein (CRP) concentration was measured, using an automated immunoturbidimetric assay, in 44 clinically normal dogs and 67 dogs with band neutrophil count greater than or equal to 10(9) cells/L, and values were found to be significantly (P less than or equal to 0.05) different. Correlation of serum CRP concentration and band neutrophil count in the 67 dogs with greater than or equal to 10(9) band neutrophils/L resulted in a statistically significant P less than or equal to 0.05), but low correlation coefficient of 0.34. Serum CRP concentration and CBC values were determined for 6 clinically normal dogs undergoing anesthesia (controls) and 6 clinically normal dogs undergoing anesthesia and ovariohysterectomy. Significant alterations in CBC results and serum CRP concentration, compared with baseline values, were lacking in dogs of the control group. Serum CRP concentration was significantly (P less than or equal to 0.05) increased above baseline values in dogs undergoing surgery and was significantly (P less than or equal to 0.05) increased, compared with values in control dogs by 12 hours after surgery. In dogs undergoing surgery, serum CRP concentration was also significantly (P less than or equal to 0.05) different from values in control dogs at 28 and 36 hours, but not at the 76- and 124-hour sample collection times. Alterations in CBC values compatible with possible or convincing inflammation were detected in 83% of the dogs undergoing surgery at the 8- and 12-hour postsurgery sample collection times, 100% of dogs at 16, 22, 28, and 36 hours after surgery, 83% of dogs at 52 and 76 hours after surgery, 67% of dogs at 100 hours after surgery, and 0% of dogs at 124 hours after surgery. It was concluded that significant increases in CRP, concentration in dogs with surgical trauma were not detected earlier than CBC alterations compatible with possible or convincing inflammation.

Serum C-reactive protein (CRP) concentration was measured, using an automated immunoturbidimetric assay, in 44 clinically normal dogs and 67 dogs with band neutrophil count greater than or equal to 10(9) cells/L, and values were found to be significantly (P less than or equal to 0.05) different. Correlation of serum CRP concentration and band neutrophil count in the 67 dogs with greater than or equal to 10(9) band neutrophils/L resulted in a statistically significant P less than or equal to 0.05), but low correlation coefficient of 0.34. Serum CRP concentration and CBC values were determined for 6 clinically normal dogs undergoing anesthesia (controls) and 6 clinically normal dogs undergoing anesthesia and ovariohysterectomy. Significant alterations in CBC results and serum CRP concentration, compared with baseline values, were lacking in dogs of the control group. Serum CRP concentration was significantly (P less than or equal to 0.05) increased above baseline values in dogs undergoing surgery and was significantly (P less than or equal to 0.05) increased, compared with values in control dogs by 12 hours after surgery. In dogs undergoing surgery, serum CRP concentration was also significantly (P less than or equal to 0.05) different from values in control dogs at 28 and 36 hours, but not at the 76- and 124-hour sample collection times. Alterations in CBC values compatible with possible or convincing inflammation were detected in 83% of the dogs undergoing surgery at the 8- and 12-hour postsurgery sample collection times, 100% of dogs at 16, 22, 28, and 36 hours after surgery, 83% of dogs at 52 and 76 hours after surgery, 67% of dogs at 100 hours after surgery, and 0% of dogs at 124 hours after surgery It was concluded that significant increases in CRP, concentration in dogs with surgical trauma were not detected earlier than CBC alterations compatible with possible or convincing inflammation.

We characterized the clinicopathologic manifestations of experimentally induced endotoxin-induced mastitis. Responses to hypertonic fluid therapy also were assessed. Eight cows received 1 mg of endotoxin by in infusion in the left forequarter. Four hours after endotoxin administration, cows received 0.9% NaCl, 5 ml/kg of body weight (n = 4) or 7.5% NaCl, 5 ml/kg (n = 4) IV. Endotoxin-infused cows had expanded plasma volume, hyponatremia, transient hyperchloremia and hypophosphatemia, increased serum glucose concentration, and decreased serum activities of liver- and muscle-specific enzymes. Calculated plasma volume increased at 6 hours in cows receiving hypertonic NaCl, and at 12, 24, and 48 hours after endotoxin infusion in both groups. Concurrent observations of decreased serum protein concentration, erythrocyte count, and hematocrit supported observations of increased plasma volume. Relative plasma volume was greater in cows receiving hypertonic NaCl (124.3%) than in cows receiving isotonic NaCl (106.6%) at 6 hours after endotoxin infusion. Cattle receiving hypertonic NaCl had increased voluntary water intake after IV fluid administration. Increased water consumption was not accompanied by increased body weight, indicating probable occurrence of offsetting body water loss. Serum sodium concentration in cows receiving hypertonic NaCl was increased 2 hours after fluid administration, but the magnitude of the change was minimal (< 4 mmol/L) and transient, indicating rapid equilibration with either interstitial or intracellular spaces. Serum sodium concentration was decreased in cows receiving isotonic NaCl at 12, 24, and 48 hours after endotoxin administration, compared with concentration prior to endotoxin administration, indicating selective loss of sodium.

We characterized the clinicopathologic manifestations of experimentally induced endotoxin-induced mastitis. Responses to hypertonic fluid therapy also were assessed. Eight cows received 1 mg of endotoxin by in infusion in the left forequarter. Four hours after endotoxin administration, cows received 0.9% NaCl, 5 ml/kg of body weight (n = 4) or 7.5% NaCl, 5 ml/kg (n = 4) IV. Endotoxin-infused cows had expanded plasma volume, hyponatremia, transient hyperchloremia and hypophosphatemia, increased serum glucose concentration, and decreased serum activities of liver- and muscle-specific enzymes. Calculated plasma volume increased at 6 hours in cows receiving hypertonic NaCl, and at 12, 24, and 48 hours after endotoxin infusion in both groups. Concurrent observations of decreased serum protein concentration, erythrocyte count, and hematocrit supported observations of increased plasma volume. Relative plasma volume was greater in cows receiving hypertonic NaCl (124.3%) than in cows receiving isotonic NaCl (106.6%) at 6 hours after endotoxin infusion. Cattle receiving hypertonic NaCl had increased voluntary water intake after IV fluid administration. Increased water consumption was not accompanied by increased body weight, indicating probable occurrence of offsetting body water loss. Serum sodium concentration in cows receiving hypertonic NaCl was increased 2 hours after fluid administration, but the magnitude of the change was minimal (< 4 mmol/L) and transient, indicating rapid equilibration with either interstitial or intracellular spaces. Serum sodium concentration was decreased in cows receiving isotonic NaCl at 12, 24, and 48 hours after endotoxin administration, compared with concentration prior to endotoxin administration, indicating selective loss of sodium.

During the hunting season of 1992, 322 black bears from Pennsylvania were examined for Toxoplasma gondii- and Trichinella spp-induced infections. Toxoplasma gondii antibodies were found in 79.8% of 322 bears--titer < 1:25 in 65 (20.2%), 1:25 in 18 (5.6%), 1:50 in 11 (34.5%) and 1:500 in 128 (38.7%) bears--by use of the modified agglutination test. Muscle tissues from 89 of these bears were bioassayed for T gondii parasites. Muscles from 64 bears, including heart from 1 bear, and heart alone from another bear, were digested in pepsin, and the digested samples were bioassayed in mice. Toxoplasma gondii was isolated from 5 bears; from the heart of 1, heart and skeletal muscles of 1, and skeletal muscles of 3. The T gondii antibody titers for the 5 bears with detectable T gondii were: greater than or equal to 1:25 in all 5 bears by use of the modified agglutination test; < 1:10 (3 bears, considered Toxoplasma-negative), 1:20 and 1:320 by use of the Sabin-Feldman dye test; < 1:64 (3 bears, considered Toxoplasma-negative), 1:128, 1:512 by use of the indirect hemagglutination test, and < 1:16 (2 bears, considered Toxoplasma-negative), 1:32, 1:64, and 1:512 by use of the latex agglutination test. Toxoplasma gondii was not isolated from feces of 5 cats fed muscles from the remaining 25 bears with T gondii antibody titer < 1:25. Tissue cysts of the 4 T gondii isolates from bears were rendered noninfective by freezing at -13 C. Antibodies against Trichinella spp were found in 6 (1.8%) of 319 bear sera; Trichinella spp larvae were detected in muscle digests of 2 of 63 bears, and in histologic sections of muscles from 3 of 162 bears. Genetic typing indicated that the 2 Trichinella isolates from bears were a sylvatic genotype and were not the species found in domestic pigs.

During the hunting season of 1992, 322 black bears from Pennsylvania were examined for Toxoplasma gondii- and Trichinella spp-induced infections. Toxoplasma gondii antibodies were found in 79.8% of 322 bears--titer < 1:25 in 65 (20.2%), 1:25 in 18 (5.6%), 1:50 in 11 (34.5%) and 1:500 in 128 (38.7%) bears--by use of the modified agglutination test. Muscle tissues from 89 of these bears were bioassayed for T gondii parasites. Muscles from 64 bears, including heart from 1 bear, and heart alone from another bear, were digested in pepsin, and the digested samples were bioassayed in mice. Toxoplasma gondii was isolated from 5 bears; from the heart of 1, heart and skeletal muscles of 1, and skeletal muscles of 3. The T gondii antibody titers for the 5 bears with detectable T gondii were: greater than or equal to 1:25 in all 5 bears by use of the modified agglutination test; < 1:10 (3 bears, considered Toxoplasma-negative), 1:20 and 1:320 by use of the Sabin-Feldman dye test; < 1:64 (3 bears, considered Toxoplasma-negative), 1:128, 1:512 by use of the indirect hemagglutination test, and < 1:16 (2 bears, considered Toxoplasma-negative), 1:32, 1:64, and 1:512 by use of the latex agglutination test. Toxoplasma gondii was not isolated from feces of 5 cats fed muscles from the remaining 25 bears with T gondii antibody titer < 1:25. Tissue cysts of the 4 T gondii isolates from bears were rendered noninfective by freezing at -13 C. Antibodies against Trichinella spp were found in 6 (1.8%) of 319 bear sera; Trichinella spp larvae were detected in muscle digests of 2 of 63 bears, and in histologic sections of muscles from 3 of 162 bears. Genetic typing indicated that the 2 Trichinella isolates from bears were a sylvatic genotype and were not the species found in domestic pigs.