The relationship between histologic lesions in endometrial biopsy specimens and susceptibility to chronic uterine infection (CUI) in mares was investigated. Mares were allotted to 4 groups on the basis of degree of endometrial lesions. Mares in group 1 (n = 6) had no pathologic changes, mares in group 2 (n = 5) had only mild pathologic changes, group-3 mares (n = 7) had moderate changes, and group-4 mares (n = 7) had severe inflammatory and fibrotic endometrial changes. Susceptibility to CUI was determined by the inflammatory response to intrauterine inoculation of 5 X 10(6) Streptococcus zooepidemicus. The inoculum was given on the third day of behavioral estrus and in the presence of a follicle > 30 mm. Mares with > 1 neutrophil/5 high-magnification (400 X) microscopic fields and > 20 colonies of S zooepidemicus at 96 hours after inoculation were considered to be susceptible to CUI. There was a significant association between biopsy grade and susceptibility to CUI among the groups. Histologically normal endometrium was associated with resistance to CUI, and severe histopathologic changes in the endometrium were associated with susceptibility to CUI. Mild to moderate endometrial lesions did not correlate consistently with susceptibility or resistance to CUI.

Streak retinoscopy was performed by 5 ophthalmologists on 256 eyes (191 dogs) to determine their postoperative refractive state after cataract extraction. Aphakic and pseudophakic eyes that had been implanted with 1 of 5 intraocular lenses (IOL) with dioptric powers ranging from +14.5 to +38 diopters (D) were studied. By use of ANOVA, breed and body type of dog and individual performing refraction were found to have no detectable effect on final refractive state. Mean refractive state of aphakic eyes was +14.4 +/- 2.10 D. Mean refractive state for different IOL powers was as follows: +14.5 D IOL = +11.54 +/- 1.18 D (n = 13); +30 D IOL = + 5.15 +/- 1.18 D (n = 105); +34.0 D IOL = +3.5 D (n = 1); +36 D IOL +2.34 +/- 0.73 D 9 (n = 61); and +38 D IOL = +1.41 +/- 0.56 D (n = 28). Residual hyperopia ranged from +0.5 D to +2.5 D with +38 D IOL, and no eyes were myopic (overcorrected) by use of any of the IOL studied. linear regression analysis of refractive state on IOL power for aU dogs predicted that dioptric strength of +41.53 D was necessary to best approximate emmetropia for the population as a whole. Body type of the dog had only slight effect (< 1.0 D) on predicted optimal IOL power. Further linear regression analysis of the 7 breeds studied predicted variations from +39.62 to +43.14 D in IOL powers necessary to approximate emmetropia. Results of the study support the routine use of canine IOL with dioptric strength of approximately +41.5 D in circumstances in which preoperative biometry and keratometry are not practical. The findings further suggest that, for the specific population of dogs studied, most of the dogs could be corrected to near emmetropia by use of a small range of IOL dioptric strengths, irrespective of body type or breed.

After a detailed anatomic study to determine puncture sites, 10 cadaver elbows from 5 dogs were examined arthroscopicalty to study the normal intraarticular anatomy, as viewed from the medial side. Subsequent dissection revealed absence of neurovascular injury and only minor iatrogenic damage to the cartilage. The technique was clinically applied and evaluated in 13 dogs (26 joints). The dogs recovered without complications. The technique proved to be safe and reliable for direct examination of nearly the entire joint. More specifically, it allowed systematic inspection of the medial and lateral humeral condyles, the medial and lateral coronoid processes, the caudal and middle parts of the head of the radius, the olecranon (including the anconeal process), and the medial collateral ligament.

To investigate the feasibility of using changes in body or mammary temperature to detect mastitis, radiotransmitters were implanted midway between rear udder quarters and in the peritoneal cavity of 5 Holstein cows (1 to 3 months in lactation) housed in an environmental chamber (16 +/- 2 C; lights on 7:00 AM to 11:00 PM). After a 6-week control period, Escherichia coli endotoxin (0.5 mg) was injected after the morning milking into left rear teat cisterns via the teat canal. Wisconsin mastitis test score and somatic cell count in all quarters increased significantly (P < 0.01) by the next milking. Effects were greatest in the endotoxin-exposed quarters. Milk yields for all quarters decreased significantly (P < 0.01) by the first milking after endotoxin injection. Udder and body temperatures at milkings were similar and were not affected by treatment. When temperatures were averaged for the 5 cows for each of 120 time points/d, average temperatures, relative to time of injection of endotoxin, were increased by 0.5 C above baseline at 2.75 hours, peaked at + 2.9 C at 6.50 hours, and remained high through 9.25 hours after injection. Power spectra calculated for individual cows on a daily basis universally indicated an increase in power at low frequencies on the day of injection. Subsequently, Streptococcus agalactiae (200 colony-forming units) was injected into right rear teat cisterns. Wisconsin mastitis test score increased at the second milking after injection. Cell count and quarter milk yield decreased by the third milking. As with endotoxin, injection of S agalactiae could not be detected via a change in temperature at milkings. Of the 5 cows, 3 had a peak in temperature after injection of S agalactiae. Average temperatures for these 3 cows relative to time of injection, were increased by 0.5 C above baseline at 24.25 hours, peaked at + 1.4 C at 26.25 hours, and remained high through 28.75 hours after injection. Power spectra calculated for the day in which a temperature peak was detected for these 3 cows indicated an increase in power at low frequencies, compared with spectra for all other days. Similar increases in power were also detected for the 2 cows that did not have temperature peaks. When clinical signs of mastitis are obvious at milking, there is little advantage of using body temperature for detection of infection. When clinical signs are not obvious, body temperature is often only minimally increased. Thus, monitoring body temperature at milkings adds little to the ability to detect mastitis. Of more interest is the ability to detect transient temperature increases that often develop in association with less-severe infections. Also, as early treatment increases the likelihood of successful treatment, detection of the onset of temperature increases would be advantageous for treatment of severe infections. Detection of a transient temperature peak requires taking temperature readings every 2 hours. To detect mastitis when a temperature peak does not occur requires measurement every 15 minutes to calculate power spectra. The ability to detect the onset of acute clinical infections and subclinical infections, using frequent temperature readings, indicates that development of a practical radiotelemetry system for use on farms may be warranted, depending on cost. The added potential of using body temperature to monitor general health and to detect estrus enhances the economic feasibility of developing such a system.

Fourteen cats were inoculated orally with 1 of 2 infective doses of Toxocara canis to induce eosinophilia. Cats were subsequently challenge exposed twice via intraperitoneal injection with 1 of 2 T canis antigen preparations. Peritoneal lavage was performed 2 days after antigenic challenge exposure, and eosinophils in the peritoneal lavage fluid were quantified. None of the cats developed clinical signs of disease after infection. All cats developed peripheral eosinophilia after infection. Significant (P < 0.05) difference in mean eosinophil count from the lavage fluid was observed between lavage 1 (prechallenge exposure) and lavages 2 and 3 (postchallenge exposure) in both groups of cats. Significant difference in eosinophil count was not found between cats given different doses of eggs. After initial challenge exposure, significantly (P < 0.05) more eosinophils were obtained from cats given antigen preparation 2 (prep-2) than from those given antigen prep-1. This difference was no longer observed after the second challenge exposure with higher doses of either antigen prep-1 or prep-2. In cats given antigen prep-2, significant difference was not found between lavages 2 and 3. However, in cats given antigen prep-1, eosinophil count was significantly (P = 0.005) greater in fluid obtained from lavage 3, compared with eosinophil count from lavage 2. Mean +/- SEM percentage of eosinophils in the fluid from lavage 3 in all cats was 70.8 +/- 2.2%. Other cell types included macrophages, neutrophils, lymphocytes, and mast cells. Gross postmortem findings were mild. One- to 3-mm nodular white foci of inflammation were observed on the serosal surfaces of the liver, spleen, kidneys, and omentum. Microscopic examination of tissues revealed pulmonary artery hypertrophy (n = 4), eosinophilic peribronchitis and perivasculitis (n = 10), mild granulomatous interstitial nephritis (n = 6), interstitial pancreatitis (n = 1), focal lymphocytic myocarditis (n = 1), focal eosinophilic granulomatous hepatitis (n = 1), and eosinophilic hyperplasia of bone marrow (n = 14). Large numbers of eosinophils could be harvested from the peritoneal cavity of cats inoculated orally with 500 embryonated T canis eggs and subsequently challenge-exposed intraperitoneally with preparations of parasite antigens. After the second challenge exposure, at least 108 eosinophils could be harvested from each cat, yielding eosinophils in the quantity required to begin isolation of granule constituents.

Serum triiodothyronine autoantibody (T3 AA), triiodothyronine (T3), and thyroxine (T4) concentrations were determined in 45 canine sera containing substantial amounts of thyroglobulin autoantibodies (Tg AA); sera also were assayed to investigate the ability of free T3 to inhibit Tg AA binding to canine Tg. Serum T3 AA concentrations defined 2 groups of sera; 28 sera had low T3 AA concentration (less than or equal to 20 ng/ml) and 17 sera had high T3 AA concentration (greater than or equal to 250 ng/ml). Direct linear correlation between T3 AA concentration and apparent serum T3 concentration was observed (r = 0.75). Serum with low T3 AA concentration had apparent T3 concentration that was significantly (P < 0.01) lower than that in serum with high T3 AA concentration. Mean serum T4 concentration was not significantly different between serum with low or high T3 AA concentration. Mean Tg AA activity was significantly (P < 0.05) lower in serum with low T3 AA concentration than in serum with high T3 AA concentration. Addition of free T3 to serum significantly (P < 0.05) decreased detectable activity of Tg AA in both groups of sera. However, significant difference in magnitude of the reduction was not observed between sera with low or high T3 AA concentration. Results indicate that a fraction of Tg AA recognizes T3-containing epitopes in Tg. Increased prevalence of T3 AA for serum with high Tg AA activity indicates that T3 AA may be another valid indicator of lymphocytic thyroiditis. These antibodies may be generated against the hormonogenic epitopes of Tg.

Two experiments were undertaken to evaluate whether porcine reproductive and respiratory syndrome (PRRS) virus was able to cross the placenta and infect midgestation fetuses following intranasal inoculation of sows and whether PRRS virus directly infected fetuses following in utero inoculation. In experiment 1, eight sows between 45 and 50 days of gestation were intranasally inoculated with PRRS virus (ATCC VR-2332), and four control sows were inoculated with uninfected cell culture lysate. Virus inoculated sows were viremic on postinoculation (PI) days 1, 3, 5, 7 and 9, shed virus in their feces and nasal secretions, and became leukopenic. Sixty-nine of 71 fetuses from principal sows euthanized on PI day 7, 14 or 21 were alive at necropsy and no virus was isolated from any of the fetuses. Two principal sows that farrowed 65 and 67 days PI delivered 25 live piglets and three stillborn fetuses. The PRRS virus was isolated from two live piglets in one litter. In experiment 2, laparotomies were performed on five sows between 40 and 45 days of gestation and fetuses were inoculated in utero with either PRRS virus alone, PRRS virus plus a swine serum containing PRRS antibodies, or uninfected cell culture lysate. Three sows were euthanized on PI day 4 and two sows on PI day 11. Viral replication occurred in fetuses inoculated with virus alone and was enhanced in fetuses inoculated with virus plus antibody. No virus was isolated from control fetuses. The results indicate that sows and fetuses are susceptible to PRRS virus infection in mid-gestation, that viral replication is enhanced by the addition of serum with PRRS virus antibody, and that the virus does not readily cross the placental barrier during mid-gestation.

A suction blister technique was used in 10 healthy dogs to remove the epidermis from the dermis in a standardized way. Collection chambers were attached to these skin windows and filled with autologous serum to attract exudative neutrophils. The chambers were emptied by fine-needle aspiration at 4-hour intervals and were refilled with serum for 24 hours after the Int aspiration. The collected cells were counted, differentiated, and stained, using the trypan blue dye-exclusion method to determine cell viability. Multiple skin biopsy specimens obtained during the procedure were examined histologically. The chamber fluid collected after 24 hours was cultured for bacteria. Increasing numbers of viable neutrophils were collected during the 24-hour period from the induced skin windows. In all but 1 dog, sufficient viable neutrophils could be collected to perform further functional tests in vitro. Our conclusion is that this technique might be useful to study chemotaxis in vivo and to perform functional tests on exudative neutrophils.

A method of extracting bacterial DNA from swine feces was developed and used in a molecular assay for the presence of ileal symbiont (IS) intracellularis, formerly known as the Campylobacter-like organism associated with swine with proliferative enteritis. Hybridization with a digoxigenin-labeled, IS intracellularis-specific probe detected the presence of IS intracellularis at a concentration of 10(7) organisms/g of feces. This method was sufficient to detect is intracellularis in the feces of swine with experimentally induced and naturally acquired infection. Results of the hybridization were in agreement with those from histologic postmortem examination.

We investigated the influence of parasympathetic tone on the arrhythmogenic dose of dobutamine in horses premedicated with xylazine, anesthetized with guaifenesin and thiamylal, and maintained on halothane in oxygen. Six horses were used in 12 randomized trials. In each trial, after end-tidal halothane concentration was stabilized at 1.1% (1.25 times minimum alveolar concentration [MAC]) in oxygen, either saline solution (0.02 ml/kg of body weight) or atropine (0.04 mg/kg) was administered IV. Five minutes later, dobutamine infusion was started at dosage of 2.5 micrograms/kg/min, IV. The dobutamine infusion was continued for 10 minutes, or until 4 or more premature ventricular complexes occurred within 15 seconds, or sustained narrow-complex tachyarrhythmia clearly not sinus in nature occurred. If the criteria for termination were not met, dobutamine infusion was increased by 2.5 micrograms/kg/min, after the hemodynamic variables had returned to baseline. The horses were allowed to recover, and were rested for at least 1 week before the second trial. The arrhythmogenic dose of dobutamine was calculated by multiplying the infusion rate by the elapsed time into infusion when arrhythmia occurred. There was significant difference between the arrhythmogenic dose of dobutamine (ADD) in saline-treated horses (mean +/- SEM, ADD 105.6 +/- 16.3 micrograms/kg) and atropinized horses (ADD 36.2 +/- 8.7 micrograms/kg). There were no differences in the prearrhythmia or immediate postarrhythmia ventricular heart rate (HR) or systolic (SAP), diastolic (DAP), or mean (MAP) arterial pressures between treated and control groups. The change in hemodynamic variables from prearrhythmia to immediate postarrhythmia formation was not different between the 2 groups. Ventricular beats were clearly evident in 8 of the 12 arrhythmias meeting the criteria for establishing the ADD. These results indicate that atropine may lower the arrhythmogenic threshold for dobutamine in halothane-anesthetized horses.