The innervation of the levator ani and coccygeal muscles and the external anal sphincter was studied by anatomic dissection in 6 clinically normal male dogs and by electrical stimulation in 5 clinically normal male dogs. Variations in innervation occasionally were found that were comparable to those reported in previous studies. Electromyographic recordings were made from the levator ani and coccygeal muscles and from the anal sphincter in 40 dogs during perineal hernia repair. Spontaneous potentials of 4 types were found in 35 dogs: fibrilation potentials, positive sharp waves, complex repetitive discharges, and fasciculations. Biopsy specimens of the cranial part of the levator ani muscle were taken in 12 dogs during perineal hernia repair. Histologic examination revealed atrophy in 7 specimens. Spontaneous potentials were recorded from all muscles with histologic evidence of atrophy. All examinations of the levator ani muscle concerned the cranial, part of this muscle, because the caudal part was absent in all 40 dogs. From combined results of electromyography and histologic examination, it was concluded that atrophy of the muscles of the pelvic diaphragm, which develops in some dogs with perineal hernia, is likely to be of neurogenic origin. Nerve damage is localized in the sacral plexus proximal to the muscular branches of the pudendal nerve or in the muscular branches separately.

A nerve muscle pedicle (NMP) graft was placed in the cricoarytenoideus dorsalis (CAD) muscle of 6 horses with induced left laryngeal hemiplegia. The NMP graft was created by use of the first cervical nerve and omohyoideus muscle. In 1 horse (control), the first cervical nerve was transected after placement of the NMP graft. One year after the surgical procedure, horses were examined endoscopically and then anesthetized. While the larynx was observed endoscopically, the first cervical nerve was stimulated. Horses were subsequently euthanatized, and the larynx was harvested. Prior to anesthesia, the endoscopic appearance of the larynx of all horses was typical of laryngeal hemiplegia. During anesthesia, stimulation of the first cervical nerve produced vigorous abduction of the left arytenoid in principal horses but not in the control horse. The right cricoarytenoideus lateralis and CAD muscles were grossly and histologically normal. Also, the left cricoarytenoideus lateralis was atrophic in all horses as was the left CAD muscle of the control horse. In contrast, the left CAD muscle harvested from principal horses had evidence of reinnervation with type 1 or type 2 fiber grouping. One year after the NMP graft procedure, horses with left laryngeal hemiplegia had reinnervation of the left CAD muscle. In another study, reinnervation was sufficient to allow normal laryngeal function during exercise. Combined, these data suggest that the NMP graft procedure is a viable technique for the treatment of left laryngeal hemiplegia in horses.

Morphologic changes in the small intestine were investigated during development of naturally acquired wheat-sensitive enteropathy in Irish Setters. To distinguish underlying morphologic abnormalities from non-specific effects of intestinal damage, progeny of affected dogs reared on a normal wheat-containing diet were compared with their own littermates reared on a cereal-free diet and with age-matched clinically normal Irish Setters fed the same wheat-containing diet. Peroral jejunal biopsy specimens were taken sequentially between 4 months and 1 year of age. At 4 months of age, there were no differences in villus height, comparing the 3 groups, but increased numbers of intraepithelial lymphocytes and goblet cells were already present in biopsy specimens from the affected Irish Setters fed wheat. Dietary wheat resulted in a progressive reduction in virus height in the jejunum of affected Irish Setters from 6 months onward. Underlying morphologic abnormalities were not found, and the characteristic morphologic changes of this enteropathy were secondary to the presence of dietary wheat. However, development of partial villus atrophy was preceded by increased numbers of intraepithelial lymphocytes and goblet cells.

OBJECTIVE To histologically evaluate and compare features of myofibers within the elongated soft palate (ESP) of brachycephalic and mesocephalic dogs with those in the soft palate of healthy dogs and to assess whether denervation or muscular dystrophy is associated with soft palate elongation. SAMPLE Soft palate specimens from 24 dogs with ESPs (obtained during surgical intervention) and from 14 healthy Beagles (control group). PROCEDURES All the soft palate specimens underwent histologic examination to assess myofiber atrophy, hypertrophy, hyalinization, and regeneration. The degrees of atrophy and hypertrophy were quantified on the basis of the coefficient of variation and the number of myofibers with hyalinization and regeneration. The specimens also underwent immunohistochemical analysis with anti-neurofilament or anti-dystrophin antibody to confirm the distribution of peripheral nerve branches innervating the palatine myofibers and myofiber dystrophin expression, respectively. RESULTS Myofiber atrophy, hypertrophy, hyalinization, and regeneration were identified in almost all the ESP specimens. Degrees of atrophy and hypertrophy were significantly greater in the ESP specimens, compared with the control specimens. There were fewer palatine peripheral nerve branches in the ESP specimens than in the control specimens. Almost all the myofibers in the ESP and control specimens were dystrophin positive. CONCLUSIONS AND CLINICAL RELEVANCE These results suggested that palatine myopathy in dogs may be caused, at least in part, by denervation of the palatine muscles and not by Duchenne- or Becker-type muscular dystrophy. These soft palate changes may contribute to upper airway collapse and the progression of brachycephalic airway obstructive syndrome.

The objective of this study was to identify the causative agents of hepatitis observed in broiler chickens at processing. Livers of chickens from 16 broiler farms in Saskatchewan with gross lesions of hepatitis were collected at processing. In addition to routine bacterial isolation and histopathological examination, serologic studies for infectious bursal disease virus (IBDV) and Chicken anaemia virus (CAV), calculation of the ratio of the weight of the bursa of Fabricius (BF) to body weight (BBW), and histopathological examination of the BF were done. Of the 264 livers with gross lesions, 83% had multifocal to coalescing necrotizing hepatitis, 16% had perihepatitis, and 1% had hemorrhages. No definitive causative microorganisms were isolated from the hepatic lesions; however, no significant bacterial isolations were made. Bursal atrophy, low BBW ratio, and high titer of antibody against IBDV each correlated with the rate of total condemnations (P = 0.0188, P = 0.0001, and P = 0.0073, respectively). Nucleotide sequencing of IBDV isolated from the BF identified the variant strains Delaware-E and 586. Condemnation because of hepatic lesions was correlated with titer of antibody against IBDV and BBW (P = 0.016 and P = 0.027). The results of this study demonstrate that hepatic lesions in Saskatchewan chickens are not currently caused by a primary bacterial pathogen but are associated with indicators of immunosuppression that is likely due to variant IBDV.

The objective of this study was to experimentally infect calves with bovine viral diarrhea virus (BVDV) isolated from free-ranging white-tailed deer. Twelve colostrum-deprived male Holstein calves were used. Eight were inoculated intranasally with a BVDV type 1a isolated from free-ranging white-tailed deer, and the other four were inoculated with the cell culture medium only and served as a control group. Whole blood, saliva, and nasal and rectal secretions were collected on days 0, 3, 7, 10, 14, 17, and 21 after inoculation for virus isolation and real-time reverse-transcriptase polymerase chain reaction (RT-PCR). On days 14 and 21, 4 calves in the infected group and 2 in the control group were euthanized; multiple tissue samples were collected for histopathologic study. Histopathologic changes included thymic atrophy and lymphoid depletion of the Peyer's patches in all 8 infected calves. The RT-PCR gave positive results with the buffy coat of all 8 infected calves, the nasal samples of 7, and the saliva samples of 2. Virus neutralization testing of the serum gave positive results for 4 of the 8 infected calves, and enzyme-linked immunosorbent assay of the serum gave positive results for 3. All of the samples from the control calves yielded negative results.

Objective-To compare experimentally induced concurrent infection with bovine viral diarrhea virus (BVDV) and bovine rotavirus (BRV) with infection of either virus alone in calves. Animals-Seventeen 1-day-old gnotobiotic calves. Procedure-Calves were allotted to 8 treatments as follows: group 1, mock-infected control calves (n = 2); group 2, inoculated with BVDV on day 1 (2); groups 3, 5, and 7, inoculated with BRV on days 1 (2), 4 (1), or 7 (2), respectively; and groups 4, 6, and 8, inoculated with BVDV on day 1 and with BRV on days 1 (2), 4 (2), or 7 (4), respectively. Concentrations of BVDV in serum and ileal tissues were measured, and BRV shedding in feces was determined. Histologic examination and immunohistochemical analysis were conducted to detect lesions and viral antigens. Results-Neonatal calves inoculated with BVDV alone or with BVDV on day 1 and BRV on day 7 developed villus atrophy and submucosal inflammation of the intestines. Concurrent BVDV and BRV infections acted synergistically in the intestinal tract, causing more severe enteric disease than infection with either virus alone. Severe lymphoid depletion was associated with BVDV infection in calves regardlesss of concurrent BRV infection. Conclusions and Clinical Relevance-Infection with BVDV played direct and indirect roles in enteritis in neonatal calves, causing villus atrophy in the duodenum and submucosal inflammation of the intestines. Also, BVDV potentiated effects of BRV. Concurrent infection with BVDV and BRV resulted in more severe enteric disease in neonatal calves than infection with BRV or BVDV alone.

Macromolecular permeability of the small intestine was tested in four 3-week-old gnotobiotic pigs inoculated with porcine rotavirus strain RV277 (group A). Pigs were administered 125I-labeled polyvinylpyrrolidone (molecular weight [mol wt], 40,000) orally 1 day before and 2 and 24 hours after virus inoculation, and blood samples were obtained every 6 hours. Eight hours after rotavirus inoculation, pigs had watery diarrhea. Increased permeation of 125I-labeled polyvinylpyrrolidone was not observed after clinical signs of infection had developed. Serum total protein and urea nitrogen concentrations increased slightly at the end of the study, probably as a consequence of dehydration. Differences in blood glucose concentration were not seen. At 48 hours after viral inoculation, macromolecular permeability was tested morphologically by injecting horseradish peroxidase (mol wt, 40,000) into the jejunal lumen just distally to the ligamentum colicoduodenale. After an incubation period of 20 minutes, small segments of jejunum were obtained for stereomicroscopic, histologic, and ultrastructural investigations. Moderate hyperregenerative villus atrophy was found. Ultrastructural changes of the villus epithelium were minor, and increased macromolecular permeation was not observed.

Transverse sections of snouts from 171 cross-bred (principally Yorkshire X American Landrace) pigs were evaluated for evidence of turbinate atrophy by use of conventional (atrophic rhinitis [AR] score) and morphometric methods. Of the 171 pigs, 35 were clinically normal (AR score, 0), 65 had mild AR (AR score, 1), 41 had moderate AR (AR score, 2), and 30 had severe AR (AR score, 3). Turbinate cross-sectional area (TA) and the ratio of TA to nostril cross-sectional area, called turbinate area ratio (TAR), had the lowest correlations (r = 0.24 to 0.55) with conventional AR score. Among clinically normal pigs, TA was greater in older pigs as expected, but the TAR values also were significantly (P less than 0.0001) different betwee n 15-week-old pigs (55 kg) and 22-week-old pigs (100 kg). Turbinate perimeter and turbinate perimeter ratio (TPR) were not influenced by pig age or source. The TPR values were closely correlated with subjective visual AR scores (r = 0.73), with AR scores derived by measuring the space between the ventral portion of the scroll and the floor of the nasal cavity (r = 0.72), and the actual size of this space in millimeters (r = 0.71). Mean TPR values for pigs assigned visual AR scores of 0, 1, 2, or 3 were 1.54, 1.25, 0.97, and 0.73, respectively. The 95% confidence intervals around these mean TRP values were discreet and did not overlap. Turbinate perimeter ratio, therefore, may be a more reliable morphometric measure of atrophic rhinitis and also provides parametric data suitable for quantitative analysis.