The pharmacokinetics and estimated bioavailability of amoxicillin were determined after IV, intragastric, and IM administration to healthy mares. After IV administration of sodium amoxicillin (10 mg/kg of body weight), the disposition of the drug was best described by a 2-compartment open model. A rapid distribution phase was followed by a rapid elimination phase, with a mean +/- SD half-life of 39.4 +/- 3.57 minutes. The mean volume of distribution was 325 +/- 68.2 ml/kg, and the mean body clearance was 5.68 +/- 0.80 ml/min.kg. It was concluded that frequent IV administration of sodium amoxicillin would be required to maintain therapeutic plasma concentrations of amoxicillin, and thus, the use of this dosage form should be limited to the initiation of treatment or to intensive care situations. After intragastric administration of amoxicillin trihydrate (20 mg/kg), 5% cherry-flavored suspension, the drug was rapidly, but incompletely, absorbed and rapidly eliminated (mean half-life of the decline phase of the plasma amoxicillin concentration-time curve, 51 minutes). The mean estimated bioavailability (fractional absorption) of the administered dose was 10.4%, and the mean peak plasma amoxicillin concentration was 2.73 microgram/ml at 1.5 hours after dosing. In one horse with clinical signs of abdominal discomfort and diarrhea, the absorption of amoxicillin from the gastrointestinal tract was delayed and the fraction absorbed was increased. It was concluded that this oral dosage form could be recommended only for the treatment of infections caused by bacteria that are highly susceptible to amoxicillin, that frequent dosing would be necessary, and that absorption may be inconsistent in horses with gastrointestinal disease. In 2 subsequent phases, amoxicillin trihydrate (10 mg/kg) was administered IM as either a 10% (100 mg/ml) or a 25% (250 mg/ml) aqueous suspension. For both formulations, plasma amoxicillin concentration peaked 45 minutes after dosing (2.08 microgram/ml for the 10% suspension and 0.98 microgram/ml for the 25% suspension). Thereafter, mean amoxicillin concentrations > 0.5 microgram/ml persisted for 24 hours, and the values achieved with the 10% suspension were approximately twice as high as those achieved with the 25% suspension throughout the sample collection period. It was estimated that absorption was complete (100%) within 24 hours after IM administration of the dose as 10% aqueous suspension, but was incomplete by 24 hours after administering the same dose as a 25% suspension. This suggests that a large portion of the latter dose remained as a precipitate at the injection site. It was concluded that amoxicillin trihydrate should be administered IM to horses as a 10%, rather than a 25%, suspension. A dosage of 10 mg/kg administered at 12-hour intervals should maintain plasma concentrations > 1 microgram/ml and should be effective in treating infections caused by bacteria that are inhibited by low concentrations of amoxicillin. This dosage regimen does not constitute broad-spectrum treatment and may be limited by the relatively large injection volume and the discomfort associated with administration.

Comparisons were made among rapid latex agglutination test and conventional biochemical tests used to identify Streptococcus agalactiae and Staphylococcus aureus. Ninety-eight streptococci and 149 staphylococci isolated from bulk tank milk were tested. Sensitivity and specificity for the latex agglutination test used for identification of Str agalactiae were 97.6 and 98.2%, respectively. Sensitivity and specificity for the latex agglutination test used for identification of S aureus were 90.2 and 67.5%, respectively. Of 25 staphylococci considered false-positive by the latex agglutination test, 14 (56%) were considered tube coagulase-positive. Fifteen staphylococci considered false-positive by latex agglutination test had biotypes representative of S hyicus or S xylosus.

Calves, 90 to 130 days old, were inoculated with bovine herpesvirus-1 (BHV-1) or parainfluenza-3 (PI-3) virus. Pulmonary lavage specimens obtained from calves before virus inoculation contained 98% alveolar macrophages (AM) and 1% neutrophils. Six days after inoculation, the mean percentage of neutrophils in lavage specimens had significantly increased to 7.9 +/- 6.0% in BHV-1-inoculated calves and to 18.3 +/- 9.9% in PI-3 virus-inoculated calves, reflecting viral-induced pulmonary inflammation that was confirmed histologically. Approximately 75% of AM obtained before virus inoculation had Fc surface receptors, and 60% had C3b receptors. Six days after inoculation, the percentage of AM with Fc and C3b receptors was significantlyreduced to 69.7 +/- 8.6% and 27.1 +/- 19.8%, respectively, in BHV-1-inoculated calves and to 67.8 +/- 15.4% and 38.8 +/- 23.2%, respectively, in PI-3 virus-inoculated calves. Alveolar macrophages obtained after virus inoculation were significantly impaired in their ability to phagocytize opsonized Staphylococcus epidermidis, but were able to kill ingested bacteria. Alveolar macrophage dysfunctions caused by BHV-1 or PI-3 respiratory infection did not differ appreciably.

Various techniques were used to look for protective, non-cross-reactive antibodies in the sera of cats exposed to virulent feline infectious peritonitis virus (FIPV). Antibodies reactive with feline enteric coronavirus (FECV) from FIPV-exposed cats were adsorbed by several passages over an FECV-Sepharose column. In an ELISA against FECV and FIPV, the activity against both viruses was removed at the same rate; thus, no FIPV-specific antibodies could be identified. By gel electrophoresis-derived ELISA, the responses of cats surviving FIPV exposure were compared with those of cats succumbing to FIPV exposure to determine whether survival could be correlated with an antibody response against a particular virus protein. Results indicated that both groups responded in the same way to the matrix envelope protein and nucleocapsid proteins. Even though the response to peplomer in each group was weak, the survivor group responded better to this protein. Furthermore, the response of this group to the peplomer protein had the highest correlation with virus neutralization titer.

In 25 adult dogs of various breeds, recurrent laryngeal nerve fibers were electrically stimulated at 2 points along their extralaryngeal course. Evoked compound muscle action potentials were recorded in this ipsilateral intrinsic laryngeal muscles, using a percutaneous needle electrode. Latencies, amplitudes, and durations were measured. Latencies were correlated with neck length (r = 0.88 on left and 0.82 on right). Five of the dogs were euthanatized, and the nerve length between the 2 stimulating needle electrodes was measured; calculated conduction velocities (mean +/- SD) were 55 +/- 6 m/s (left) and 57 +/- 6 m/s (right). In 38 additional canine cadavers, the lengths of the exposed left and right recurrent laryngeal nerves were correlated with neck length (r = 0.44 on left and 0.56 on right). A linear regression model is proposed for predicting normal latencies, despite variations in neck length among different breeds of dogs.

Feline immunodeficiency virus (FIV; formerly, feline T-lymphotropic lentivirus) is a typical lentivirus resembling human and simian immunodeficiency viruses in morphologic features, protein structure, and reverse transcriptase enzyme. It is antigenically dissimilar, however. The virus is tropic for primary and permanent feline T-lymphoblastoid cells and Crandell feline kidney cells. The virus did not grow in other permanent feline non-lymphoblastoid cells that were tested or in lymphoid and non-lymphoid cells from man, dogs, mice, and sheep. During short term inoculation studies in cats, the feline immunodeficiency-like syndrome found in nature was not experimentally induced, but a distinct primary phase of infection was observed. Fever and neutropenia were observed 4 to 5 weeks after inoculation; fever lasted several days, and neutropenia persisted from 1 to 9 weeks. Generalized lymphadenopathy that persisted for 2 to 9 months appeared at the same time. Antibodies to FIV appeared 2 weeks after inoculation and then plateaued. Virus was reisolated from the blood of all infected cats within 4 to 5 weeks after inoculation and persisted indefinitely in the face of humoral antibody response. Virus was recovered from blood, plasma, CSF and saliva, but not from colostrum or milk. Contact transmission was achieved slowly in one colony of naturally infected cats, but not between experimentally infected and susceptible specific-pathogen-free cats kept together for periods aslong as 4 to 14 months. The infection was transmitted readily, however, by parenteral inoculation with blood, plasma, or infective cell culture fluids. In utero and lactogenic transmission were not observed in kittens born to naturally or experimentally infected queens. Lymphadenopathy observed during the initial stage of FIV infection was ascribed to lymphoid hyperplasia and follicular dysplasia. A myeloproliferative disorder was observed in 1 cat with experimentally induced infection.

Pig epizootic diarrhea virus cannot be grown in cell culture; for its characterization, intestinal perfusate material from a pig infected with the strain CV777 had to be used. In isopyknic sucrose gradients, a peak of virus-specific ELISA activity was detected at a density of 1.17 g/ml. Using immunoprecipitation of radioiodinated-purified virus material followed by sodium dodecyl sulfate-polyacrylamide gel electrophoresis, 3 proteins of low molecular weight (20,000 to 32,000 daltons [D] were found; after blotting nitrocellulose and glycoprotein identification with concanavalin A and horseradish peroxidase, 1 of the proteins (23,000 D) gave a signal. Another protein of 58,000 D was encountered, which was the only protein binding an RNA probe. Finally, a protein of 85,000 D was visible, associated with minor bands of about 110,000 and 135,000 D in most experiments. Using the concanavalin A-blotting technique, the same bands were visualized. The demonstration of a polydisperse cluster of proteins from 20,000 to 32,000 D (of which at least 1 is glycosylated), of glycosylated proteins from 85,000 to 135,000 D, and of an RNA-binding protein of 58,000 D is taken as structural evidence that pig epizootic diarrhea virus should be classified with the Coronaviridae, irrespective of the apparent lack of an antigenic relationship with other members of that family.

We attempted to determine whether weaning is required for induction of diarrhea in pigs with postweaning enterotoxigenic Escherichia coli infection. Three-week-old newly weaned pigs and their suckling littermates were inoculated with the K88+ enterotoxigenic E coli strain M1823B. Fourteen of 21 weaned and 12 of 20 suckling pigs were genetically resistant to intestinal adhesion by the K88+ strain of E coli; they remained healthy, and gained weight at similar rates. Both groups of K88-resistant pigs gained weight faster, and shed fewer bacteria of strain M1823B in their feces, than did their K88-susceptible counterparts. Diarrhea developed in K88-susceptible pigs in the weaned (6 of 7 pigs) and suckling (4 of 8 pigs) groups, and 1 of the 4 affected suckling pigs died from complications resulting from diarrhea. The incidences of diarrhea, weight gain rates, and the numbers of strain M1823B shed in feces of susceptible weaned and suckling pigs were not significantly (P > 0.05) different. Diarrhea scores of susceptible weaned pigs were significantly (P < 0.02) higher than those of susceptible suckling pigs on the second day after inoculation. In this experimental model, it was concluded that weaning is not required for induction of diarrhea, but may modestly increase its severity.

Microvascular permeability characteristics were evaluated in digits of 7 adult horses. After capillaries were isolated and an extracorpeal perfusion circuit for the digit was established, a lymphatic vessel draining the distal portion of the phalangeal region was cannulated at the level of the coronary band. Venous pressure was increased in a stepwise manner, and lymph flow, lymph protein concentration (Cl), and plasma protein concentration (Cp) were determined after measured variables were allowed to reach steady state. Lymph-to-plasma protein concentration ratios (Cl/Cp) and lymph and plasma oncotic pressures were determined from samples collected during steady state. The osmotic reflection coefficient was determined after Cl/Cp became constant, regardless of increasing lymph flow, and was expressed as 1 - Cl/Cp. The osmotic reflection coefficient for the digit was 0.67. Seemingly, the microvasculature bed of the digit was relatively permeable and could maintain only 67% of the endogenous macromolecules within the vasculature.

The effect of low-dose challenge of immunity with pseudorabies virus (PRV) on subunit-vaccinated pigs was studied in 2 experiments. In the first experiment, we studied the effect of challenge dose on the antibody response to an early excreted 98-kilodalton PRV-glycoprotein that was used as a diagnostic antigen in the ELISA. In the second experiment, we studied the effect of low doses of virus on the establishment of latent infections in subunit-vaccinated pigs. The relationship of virus exposure dose and vaccine dose to the response of pigs to diagnostic antigen was studied in 18 pigs. Two groups of 3 pigs were vaccinated with a total of 200 micrograms of a lectin-derived PRV subunit vaccine over a 5-week period. Two groups of 3pigs were similarly vaccinated with a total of 100 micrograms. Two groups of 3 pigs served as nonvaccinated controls. One group of pigs from each of the preceding categories was intranasally exposed to 10(6.0) and 10(2.7) plaque-forming units (PFU) of virus. Antibody to diagnostic antigen was detected by the ELISA and radioimmunoprecipitation 3 to 7 days earlier in pigs exposed to 10(6.0) PFU, demonstrating that the size of the virus challenge dose affects the antibody response to diagnostic antigen. The establishment of latent infections by low PRV doses and the ability to detect these infections was studied in 10 subunit-vaccinated pigs. Each pig was intranasally exposed to 10(2.3) PFU of virus (day 0). The serum virus-neutralizing antib ody titer of these pigs increased to their highest level 14 to 21 days after exposure and then steadily decreased through day 113, indicating absence of viral recrudescence. All pigs were treated with dexamethasone for 4 consecutive days, beginning on day 113. Latent infections were identified in 8 of 10 pigs on the basis of recovery of virus and/or 2 log2 or greater increases in serum virus-neutralizing titer. Antibody to diagnostic antigen was initially detected in the 8 latently infected pigs on day 14 or 21 and continued to be detected through days 21, 46, 53, 110, and 113 in 1, 2, 1, 1, and 3 pigs, respectively. The antibody titer to diagnostic antigen increased in 6 of the 8 latently infected pigs after dexamethasone treatment. However, antibody to diagnostic antigen was not detected by ELISA in the remaining 2 latently infected pigs, despite increases in serum virus-neutralizing titers in both pigs and the recovery of reactivated virus from one pig. The failure to consistently detect antibody to diagnostic antigen in latently infected pigs suggests that diagnostic tests using nonvaccine diagnostic antigen may be suitable only for detecting infections in vaccinated herds, but not in individual pigs.