High-performance liquid chromatography (HPLC) was used to determine the phospholipid (PL) composition of ovine, equine, bovine, porcine, and canine RBC membranes. Procedural modifications of established techniques provided for separation of 7 PL within a 15- to 20-minute sample run. Significant (P < 0.05) differences were detected in RBC membrane PL composition among the various species. The concern for physiologic properties associated with hemolysis and/or sedimentation rate must include evaluation of differences in the PL bilayer structure.

The putative binding of porcine parvovirus (PPV) to semen components in vitro was examined along with the shedding pattern of PPV in oronasally infected boars. Porcine parvovirus DNA was determined to be bound to spermatozoa that had been incubated in vitro with PPV and washed to remove loosely adherent virus. To determine whether PPV was shed in the semen, four 8-month-old boars, seronegative for PPV, were inoculated oronasally with a virulent strain of PPV. Prior to virus inoculation, a catheter was surgically implanted in the vas deferens for the purpose of collecting cauda epididymal semen free of extrinsic contamination. Epididymal semen specimens were collected prior to inoculation and daily thereafter for 21 days. A fifth boar was inoculated oronasally with PPV, but semen was collected by electroejaculation twice weekly for an equal period of time. Reproductive glands and semen specimens from all boars were examined by nucleic acid hybridization for the presence of viral DNA. All boars seroconverted to PPV, as evidenced by serum antibody titers ranging from 512 to 8,192 hemagglutinating inhibition units/50 microliter. Porcine parvovirus DNA was detected in epididymal semen of 3 of 4 catheterized boars on postinoculation days 5 through 9, but not in semen obtained by electroejaculation. Viral DNA was consistently detected in tissue samples collected on postinoculation days 8 and 21 from the scrotal lymph nodes (4 of 5 boars) and epididymides (3 of 5 boars).

At an abattoir, lesion specimens from 140 condemned sheep livers were collected for bacteriologic culture and for pathologic examination. Grossly, 23 lesions were abscesses; from 9 of which, Fusobacterium necrophorum biovar A (3 in pure culture and 6 in mixed culture) was isolated and from 14 of which, biovar B (6 in pure culture and 8 in mixed culture) was isolated. Escherichia coli was the predominant facultative anaerobic bacterium and Clostridium perfringens was the predominant obligate anaerobic bacterium isolated from the 14 lesions with mixed bacterial infection. Histologically, these lesions had a core of coagulation necrosis, encircled by a zone of necrotic phagocytic cells and bacteria with cellular characteristics of F necrophorum biovars A or B, and a connective tissue capsule. Of the 117 lesions without F necrophorum, 49 were culture-positive (for other organisms) and 69 were culture-negative. These 117 lesions were fibrous and were smaller than the 23 abscesses. A variety of gram-positive and gram-negative facultative anaerobic and obligate anaerobic bacteria was isolated from the culture-positive lesions, but always in low numbers. Eleven culture-negative and 18 culture-positive lesions were examined and had histologic characteristics of parasite-induced granulomas, with numerous eosinophils and epithelioid giant cells. Results of the study indicated that the histologic appearance of ovine hepatic lesions with F necrophorum was similar to bovine liver abscesses caused by F necrophorum, but unlike bovine liver abscesses, F necrophorum biovar B was isolated more frequently than was biovar A and often in pure culture. Most of the lesions in the condemned livers were parasite-induced granulomas.

Seventeen sows were fed 1,000 Toxoplasma gondii oocysts of isolates GT-1 or PT-1 at 32 to 92 days of gestation, and the products of conception were examined for T gondii antibodies and parasites. Twelve of these sows were euthanatized near term between 21 and 62 days after being fed T gondii; fetal body fluids or fetal sera were examined for agglutinating T gondii antibodies, and tissues were bioassayed in mice for T gondii parasites. Six sows produced pigs that had been transplacentally infected with T gondii; one of them aborted a T gondii-infected fetus 17 days after ingesting oocytes. Agglutinating antibodies were detected in fetuses infected in utero, but transplacental transfer of T gondii antibodies was not observed in noninfected fetuses. Transcolostrally acquired T gondii antibodies disappeared by 3 months of age. Diagnosis of transplacental toxoplasmosis was confirmed on the basis of detection of T gondii organisms in fetal tissues by use of histologic examination and bioassay in mice. In conclusion, finding of T gondii antibodies in body fluids could serve as a rapid screening test for transplacental T gondii infection in pigs.

Ultrasonographic or anatomic observations or both were made of the kidneys of 26 dogs. The anatomic studies established precise correlations between the gross anatomic features of the organ and its ultrasonographic images obtained in transverse, sagittal, dorsal, and 2 oblique planes. Uniformily mottled echogenicity of the renal cortex could be clearly differentiated from the less echogenic renal medulla. In the middorsal plane, the papillae of the renal pyramids were directed towards the renal sinus. The bases of the pyramids were almost circular in outline in the midsagittal images and the renal crest was seen as an echogenic line. Although the renal sinus was highly echogenic, neither the renal pelvis nor its recesses were detected. The walls of each of the interlobar arteries provided echogenic parallel lines, passing in the renal recesses between the renal pyramids. Arcuate arteries were demonstrated at the corticomedullary junction and interlobular arteries were detected within the renal cortex. For the right kidney, transverse images were obtained with the ultrasonographic transducer at the last 2 intercostal spaces; images in the dorsal, sagittal, and oblique planes were obtained with the transducer placed over the caudal extremity of the kidney. In the left kidney, transverse images were made with the transducers at, and caudal to, the last intercostal space; images in the dorsal, sagittal, and oblique planes were obtained with the transducer placed over the lateral border of the kidney. The use of such a protocol ensures that the entire organ is inspected and a diagnosis of either a normal or pathologic kidney is made.

Cellular and humoral immune responses of pigs inoculated with Mycoplasma hyopneumoniae were investigated at postinoculation weeks (PIW) 2, 4, and 6. The response of blood lymphocytes (BL) and bronchial lymph node lymphocytes (LNL) to stimulation by M hyopneumoniae antigens was evaluated by a lymphocyte-stimulation test. Specific antibodies in serum and lung washing samples were assayed by ELISA. Immunoglobulin-positive cells in lungs and bronchial lymph nodes were identified by indirect fluorescent antibody test, using isotype-specific monoclonal antibodies. At PIW 0 to 6, BL from control and M hyopneumoniae-inoculated pigs were stimulated by M hyopneumoniae cells; however, BL from inoculated pigs generally had higher stimulation indices, especially at PIW 6. The response of LNL was influenced by previous exposure to M hyopneumoniae, as indicated by higher stimulation indices (P < 0.01) of LNL from inoculated pigs killed at PIW 2 and 6. Specific ELISA antibodies to M hyopneumoniae in lung washings from inoculated pigs consisted mainly of IgG and IgA isotypes. Examination of lung sections by indirect immunofluorescence revealed that cells producing IgM and IgA were in controls as well as M hyopneumoniae-inoculated pigs, but IgG-positive cells were only in lungs of inoculated pigs. Resolution of pneumonia appeared to correlate with development of increased sensitization of BL, as well as development of marked increases in immunoglobulins, particularly IgG in lung washings at PIW 6.

The genomes from field isolates of Pasteurella multocida in turkeys and those of P multocida reference CU and M9 vaccine strains were analyzed and compared after cleavage with restriction endonucleases. The electrophoretic profiles obtained with DNA fragments from field isolates and vaccine strains of the same serotype were characteristic and reproducible. These features indicated the existence of differences among the isolates of the same serotype that cannot currently be detected, using available serotyping methods. However, several field isolates had electrophoretic profiles similar to those of either CU or M9 vaccine strain. It was concluded that restriction endonuclease analysis of DNA genomes from P multocida isolated from turkeys provides the information for differentiation of field isolates from vaccine strains of the same serotype.

A panel of 40 monoclonal antibodies (MAb) specific for bovine viral diarrhea virus (BVDV) was produced, and each MAb was characterized and grouped according to its viral protein specificity, immunoglobulin subclass, virus-neutralizing activity, and immunoreactivity with a large collection of BVDV isolates. The MAb were found to be specific for 1 of 3 sets of related viral-induced proteins found in cells infected with the Singer strain of BVDV. Group-1 MAb were specific for the 80- and 118-kilodalton (kD) proteins of BVDV. Group-2 MAb recognized 3 proteins with molecular sizes of 54, 56, and 58 kD. Group-3 MAb recognized a 43- and a 65-kD protein. The MAb belonged to either the IgG1, IgG2a, IgG2b, IgG3 subclasses or the IgE class of mouse immunoglobulin. All MAb in group 2 were able to neutralize BVDV and had neutralization titers that ranged from 24 to 1,600,000. The reactivity of the MAb with numerous field isolates of BVDV was highly variable. Both cytopathic and noncytopathic biotypes of BVDV were examined and had the same degree of antigenic variation. The greatest degree of variation was detected with group-2 MAb. The data demonstrate that BVDV isolates have a high degree of antigenic variation that is largely confined to the envelope glycoproteins associated with virus neutralization. The results also suggest that antigenic variability of this virus is important in the development and severity of the disease it causes.

The chemotactic activity of turkey peritoneal macrophages in response to an atherosclerotic plaque extract from a hypertensive strain of turkeys was determined. Atherosclerotic plaque extract stimulated macrophage chemotaxis, whereas normal aortic extract did not stimulate macrophage chemotaxis. However, differences were not revealed by sodium dodecyl sulfate-polyacrylamide gel electrophoretic analysis of extracts of atherosclerotic plaque and normal aorta. Chemotactic activity was diminished with pronase treatment, suggesting the chemoattractant is a protein. Seemingly, atherosclerotic plaque of turkeys contains a macrophage chemotaxin.

Phorbol myristate acetate (PMA), which induces acute pulmonary injury in mammals, induced acute airsacculitis in turkeys after intra-airsac inoculation of 0.1 mg/kg. Grossly, air sacs contained multifocal to diffuse hemorrhage and edema at postinoculation hours (PIH) 3 and 6. Microscopically, there was multifocal congestion and small thrombocyte aggregates within small blood vessels by PIH 0.5, with a few vessels containing small numbers of marginating heterophils. By PIH 1.5, thrombocyte aggregates were larger and more numerous, and moderate numbers of heterophils were located perivascularly. Erythrocytes and proteinaceous fluid were in air sac interstitium. By PIH 3 and 6, hemorrhage and exudation of proteinaceous fluid had increased, in some instances severely distending the air sac. Ultrastructurally, changes resulting from PMA-induced injury were thrombocyte aggregation and degeneration, air sac epithelial cell vacuolation with separation of interdigitating cell processes, and endothelial cell vacuolar degeneration with loss of vascular integrity. Air sac lavage fluids had mildly increased total cell counts by PIH 1.5, but values returned to baseline by the end of the experiment, indicating lack of cell exudation into the air sac lumen. Circulating leukocyte changes included transient lymphopenia at PIH 3 and marked heterophilia at PIH 6. These results indicate that thrombocytes and/or heterophils are central to the pathogenesis of injury induced in air sacs by PMA and that the air sac responds differently to PMA than to pathogenic bacteria.