Eight of 10 pony foals reared under helminth-free conditions were inoculated PO with 50 Strongylus vulgaris infective larvae/week for 4 weeks, at which time 1 foal died of acute verminous arteritis. Inoculation of 7 remaining foals continued at 2-week intervals for 20 weeks. Of the 7 foals, 3 were treated with ivermectin (0.2 mg/kg of body weight) in an oral paste formulation at experiment weeks 8, 16, 24; 4 foals were not treated. Two foals were not inoculated or treated and served as controls. After the first ivermectin treatment, ivermectin-treated foals had fewer days (12 +/- 2.9) with rectal temperatures > 38.6 C than did nontreated foals (23.3 +/- 3.8). Mean baseline rectal temperatures were 38 +/- 0.2 C. Adverse clinical reactions to ivermectin treatment were not observed in foals. Foals were euthanatized and necropsied 3 weeks after the last ivermectin treatment (week 24). Ivermectin was effective in reducing S vulgaris arterial larval and intestinal adult parasite numbers by 100% in 3 treated foals. Strongylus vulgaris arterial larvae and/or adults were recovered from all 4 nontreated inoculated foals. One nontreated inoculated foal lacked arterial larvae or active arterial lesions, indicating that protective resistance had developed in this individual. Marked gross and histopathologic lesions typical of chronic S vulgaris infection were observed in the 3 nontreated inoculated foals with arterial larvae. Repeated killing of intra-arterial S vulgaris fourth-stage larvae in ivermectin-treated foals did not exacerbate lesions associated with verminous arteritis or induce unique lesions associated with repeated destruction of arterial larvae. Arterial lesions in treated inoculated foals were markedly reduced and had resolved, compared with those in nontreated inoculated foals.

Serum concentration of ampicillin, a semisynthetic penicillin, was measured in mares at various time intervals up to 24 hours after intrauterine infusion of 3 g of ampicillin. Blood samples were drawn immediately before infusion and at l-, 4-, 10- and 24-hour intervals after infusion. At postinfusion hour 24, two endometrial biopsy specimens were obtained to measure endometrial concentrations of ampicillin. Blood was drawn twice as part of the 24-hour postinfusion sample collection, once before removal of the biopsy specimens and again 5 minutes after removal of the biopsy specimens. After drug infusion, more diestrous mares had detectable serum ampicillin concentration than did estrous mares for all samples, except the 24-hour prebiopsy sample. None of the 24-hour prebiopsy serum samples had detectable ampicillin concentration, but ampicillin was detected in the serum of 4 of 5 diestrous mares after endometrial biopsy. Endometrial concentrations of ampicillin were detectable at postinfusion hour 24 in estrous and diestrous mares, but were not different. All 24-hour biopsy specimens had ampicillin concentrations greater than the ampicillin minimal inhibitory concentration.

Twelve biotinylated lectins and an avidin-biotin-peroxidase method were used to detect and localize specific carbohydrate residues on formalin-fixed, paraffin-embedded female canine mammary gland sections. Histologic sections from 3 lactating and 7 nonlactating mixed-breed dogs (age 5.6 +/- 0.35 years) were incubated with Arachis hypogea agglutinin (peanut agglutinin; PNA), Concanavalia ensiformis agglutinin (conA), Dolichos biflorus agglutinin (DBA), Glycine max agglutinin (SBA), Griffonia simplicifolia agglutinin-I (GS-I), Lens culinaris agglutinin (LCA), Lycopersicon esculentum agglutinin (LEA), Phytolacca americana mitogen (pokeweed mitogen; PWM), Ricinus communis agglutinin-I and-II (RCA-I and -II), Triticum vulgaris (WGA), and Ulex europaeus agglutinin-I (UEA-I). Each lectin had a specific binding pattern, except SBA and DBA. In nonlactating glands, PNA, conA, LEA, and UEA-I stained duct cells in a linear-binding pattern, with a mean percentage of positive ducts per section of 28.7 (+/- 0.6), 65.7 (+/- 0.3), 100 (+/- 0), and 8.4 (+/- 0.2), respectively. Strong apical, lateral, basal, and cytoplasmic positivity on duct cells was seen after incubation of the sections with RCA-I, RCA-II, and WGA in all ducts. In acinar cells, the binding pattern and the staining distribution of all the lectins studied were similar to those in duct cells. However, for PNA, conA, and UEA-I, the mean percentage of positive lobules per section was 33.7 (+/- 0.9), 62 (+/- 0.5), and 10.5 (+/- 0.2), respectively. In glands from lactating dogs, conA and UEA-I did not stain. The cytoplasm of all myoepithelial cells was moderately stained with RCA-I, RCA-II, and WGA. Endothelial cells stained with GS-I, PWM, RCA-I, RCA-II, WGA, conA, and LCA. The extracellular matrix, especially the periacinar and periduct regions, and the interstitial fibroblasts were positive for LCA, RCA-I, RCA-II, and WGA. Peripheral unmyelinated nerve fibers of the nipple were strongly positive for GS-I, PWM, RCA-1, RCA-II, and WGA. Some of the lectins used (ie, PNA, conA, UEA-I, GS-I, PWM, and LEA) appear to have selective staining of mammary gland structures that seems to be correlated with various physiologic functions. The contrasting binding pattern of lectins specific for the same sugar indicates a lack of knowledge of interactions between lectins and carbohydrate residues in tissue sections.

Articular cartilage specimens from the distal articular surface of 32 radiocarpal bones from 24 2- to 5-year-old horses were analyzed. The total collagen content was determined on the basis of the 4-hydroxyproline content, using a colorimetric method. A method for estimating the proportions of types-I and -II collagen by measuringspectrophotometric densities of specific cyanogen bromide peptide bands from mixtures of types-I and -II collagen on sodium dodecyl sulfate-polyacrylamide gels was used. The cyanogen bromide peptides representative of each collagen types-I and -II were identified. The peptide ratios were then computed for each of several standards of type-I and -II mixtures. A standard curve was derived from the correlation between these ratios and the corresponding proportions of type-II collagen in standard mixtures. Galactosamine and glucosamine content (hexosamines) were measured by ion chromatography. Thegalactosamine-to-glucosamine ratio, chondroitin sulfate and keratan sulfate values, and total glycosaminoglycan content were derived from the measured hexosamine content. The total collagen content averaged 556 mg/g (55.6 mg/100 mg) of tissue (dry weight, [dw]). Type-II collagen was the major collagen type in normal articular cartilage specimens. The ratio of the area under the alpha 1 (II)CB10 peak to the area under the alpha 1 (I)CB 7,8 + alpha 1 (II)CB11 peak was a second-order polynomial function of the proportion of type-II collagen in the specimens. The mean galactosamine and glucosamine content were 20.6 mg/g and 7.9 mg/g (dw), respectively. The meangalactosamine-to-glucosamine ratio was 3.74 +/- 0.62. Chondroitin sulfate values, keratan sulfate values, and total glycosaminoglycan content were 53.3 +/- 4.9 mg/g, 19.9 +/- 3.6 mg/g, and 73.2 +/- 7.9 mg/g (dw), respectively. There was no significant correlation between the age of the horses and any of the chemical values (P>0.1). The biochemical composition of articular cartilage in the horse is similar to that of other species.

In this preliminary investigation, various hematologic variables potentially influential in determining the degree of blood viscosity were evaluated in 10 Thoroughbred horses subjected to competitive acute running exercise. Following completion of sprints over a distance of 1.25 miles, mean percent (+/- SD) increases in PCV (38.3 +/- 12.9%), RBC (47.8 +/- 15.3%), and rouleaux index (232.7 +/- 176.8%) were recognized. Simultaneous increases in total plasma protein (28.3 +/- 5.31%), serum albumin (26.7 +/- 6.80%), alpha 1-globulin (60.0 +/- 49.0%), alpha 2-globulin(25.5 +/- 27.9%), beta 1-globulin (46.7 +/- 21.1%), beta 2-globulin (35.0 +/- 50.6%), gamma 1- and 2-globulins (38.7 +/- 29.6%), and plasma fibrinogen (12.5 +/- 10.4%) concentrations increased simultaneously. Horses also had consistent decreases in albumin:globulin ratio (- 10.0 +/- 7.43%). Alterations in these hematologic values after acute running exercise in Thoroughbred horses accompanied increases in serum (69.3 +/- 39.7%), plasma (39.7 +/- 11.9%), and blood (134.7 +/- 55.3%) viscosity.

Four groups of 18 beef calves each were used to evaluate effects of different treatments on parasite control and weight gains. The investigation extended from November 1986 (weaning) to October 1987. Group-1 calves were treated with ivermectin (200 micrograms/kg of body weight, SC) at approximately 6-week intervals for a total of 8 treatments; group-2 calves were given the same dosage of ivermectin by the same route of administration as group-1 calves in November, March, and July; group-3 calves were given fenbendazole paste (5 mg/kg, PO) at the same times as group-2 calves; and group-4 calves served as untreated controls with provision for ivermectin salvage treatment. All groups grazed on individual pairs of larval-contaminated, 1.6-ha pastures. Highest (P < 0.05) initial worm counts in fall tracer calves were found in group 3 (Ostertagia ostertagi and Trichostrongylus axei adults) and group 4 (O ostertagi and Haemonchus adults). Fecal egg counts of group-1 calves were low throughout the experiment and pasture larval counts remained negligible after July. Egg counts and larval counts of other groups remained higher into summer. Worm counts, including O ostertagi inhibited early fourth-stage larvae (EL4), were highest (P < 0.05) in groups-3 and -4 spring tracer calves; numbers of O ostertagi EL4 were similarly high in groups 2, 3, and 4; and T axei counts were highest (P < 0.05) in groups-3 and -4 yearlings slaughtered in spring. Liveweights of group-1 calves were greater (P < 0.05) than in other groups from March 2 to October, and by July 2, group-2 calves had a liveweight advantage over group-4 calves. Group-3 calves had the lowest rate of gain from March to July and mean liveweight of the group was less (P < 0.05) than in all other groups from April to October. Only minimal worm numbers were recovered from groups-1 or -2 calves in October. Large numbers of O ostertagi and T axei were recovered from group-4 calves and O ostertagi from group-3 calves. A few calves in groups 3 and 4, but 365 kg in group 1, 328 kg in group 2, 316 kg in group 4, and 281 kg in group 3.

The macrolytic lactone F28249-alpha was titrated in experimentally infected sheep and found to be highly effective against most of the common gastrointestinal nematodes as a single oral dose, given at a rate of 0.025, 0.05, or 0.1 mg/kg. Specifically, maximal activity was evident at even the lowest dosage against adult Haemonchus contortus, Ostertagia circumcinta, Trichostrongylus axei, and T colubriformis and L4 O circumcinta. Activity against Oesophagostomum columbianum was also high at all dosages, with a calculated ED95 of 0.029 mg/kg. Cooperia curticei was eliminated at 0.1 mg/kg, but control was erratic at the lower dosages. The greatest weakness of this compound was its activity against C oncophora. The activity against this parasite was weak (<less than or equal to 85%) at all dosages, and the dosage-response curve was flat, suggesting dosages substantially higher than those given would be necessary for high-order control of this species.

Postadulticide pulmonary hypertension mechanisms and treatment with antihistamines and supplemental oxygen were studied in eight dogs with heartworm disease. To ensure severe postadulticide thromboembolism, additional heartworms (either 20 or 40 into 4 dogs each) were transplanted into naturally infected dogs before thiacetarsamide treatment. During pentobarbital anesthesia, 2 pulmonary hemodynamic studies were conducted on each dog with a sequence of baseline, hypoxia with FlO2 = 10%, hyperoxia with FlO2 = 100%, a second baseline, treatment with either diphenhydramine (D) or cimetidine (C), and another hypoxia. All dogs were pulmonary hypertensive, with each dog having a mean pulmonary arterial pressure (PPA) greater than 20 mm of Hg. Mean PPA increased from baseline conditions (25.0 +/- 4.5 SD for D and 24.3 +/- 4.4 for C) to hypoxia (28.5 +/- 4.7 for D and 28.4 +/- 3.7 for C), and decreased during hyperoxia (16.9 +/- 3.0 for D and 17.4 +/-3.0 for C), respectively. Neither antihistamine reduced PPA at normoxia. The degree of pulmonary hypertension when breathing room air increased even more during hypoxia, and this increase was not attenuated by either antihistamine. Histamine did not appear to mediate pulmonary hypertension during postadulticide thromboembolism, nor to modify the hypoxia-mediated pulmonary hypertension at this disease stage. Because baseline PO2 was low (66.6 +/- 11.7 mm of Hg for D and 69.4 +/- 14.2 for C) and because PPA decreased during administration of oxygen, the pulmonary hypertension was mostly hypoxia-induced. In addition to the arterial lesions, much of the pulmonary hypertensive mechanism was an active and reversible vasoconstriction in response to hypoxia caused by the secondary lung disease. Supplemental oxygen to dogs with pulmonary hypertension could reduce PPA and right ventricular afterload. This study supports the use of oxygen, but not antihistamine drugs, in the treatment of postadulticide heartworm disease in dogs that are hypoxic, with signs of congestive heart failure or dyspnea.