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.

Coinfection of goose parvovirus (GPV) and duck circovirus (DuCV) occurs commonly in field cases of short beak and dwarfism syndrome (SBDS). However, whether there is synergism between the two viruses in replication and pathogenicity remains undetermined. We established a coinfection model of GPV and DuCV in Cherry Valley ducks. Tissue samples were examined histopathologically. The viral loads in tissues were detected by qPCR, and the distribution of the virus in tissues was detected by immunohistochemistry (IHC). Coinfection of GPV and DuCV significantly inhibited growth and development of ducks, and caused atrophy and pallor of the immune organs and necrosis of the liver. GPV and DuCV synergistically amplified pathogenicity in coinfected ducks. In the early stage of infection, viral loads of both pathogens in coinfected ducks were significantly lower than those in monoinfected ducks (P < 0.05). With the development of the infection process, GPV and DuCV loads in coinfected ducks were significantly higher than those in monoinfected ducks (P < 0.05). Extended viral distribution in the liver, kidney, duodenum, spleen, and bursa of Fabricius was consistent with the viral load increases in GPV and DuCV coinfected ducks. These results indicate that GPV and DuCV synergistically potentiate their replication and pathogenicity in coinfected ducks.

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.

Objective-To assess the heritability of pancreatic acinar atrophy (PAA) in German Shepherd Dogs (GSDs) in the United States. Animals-135 GSDs belonging to 2 multigenerational pedigrees. Procedure-Two multigenerational pedigrees of GSDs with family members with PAA were identified. The clinical history of each GSD enrolled in the study was recorded, and serum samples for canine trypsinlike immunoreactivity (cTLI) analysis were collected from 102 dogs. Dogs with a serum cTLI concentration ≤ 2.0 µg/L were considered to have exocrine pancreatic insufficiency (EPI) and were assumed to have PAA. Results-Pedigree I consisted of 59 dogs and pedigree II of 76 dogs. Serum cTLI concentrations were measured in 48 dogs from pedigree I and 54 dogs from pedigree II. A total of 19 dogs (14.1%) were determined to have EPI, 9 in pedigree I (15.3%) and 10 in pedigree II (13.6%). Of the 19 dogs with EPI, 8 were male and 11 were female. Conclusion and Clinical Relevance-Evaluation of data by complex segregation analysis is strongly suggestive of an autosomal recessive mode of inheritance for EPI in GSDs in the United States.

Sequential assessments of pancreatic structure and function were performed on a female German Shepherd Dog bred from parents with exocrine pancreatic insufficiency (EPI), to monitor development of pancreatic acinar atrophy in this breed. Determinations of serum trypsin-like immunoreactivity (TLI), results of N-benzoyl-L-tyrosyl-P-aminobenzoic acid test, fecal soy bean stimulation test (SST), and gross and histologic examinations of the pancreas did not provide evidence of exocrine pancreatic disease up to 13 months of age. However, electron microscopy revealed degenerative abnormalities of acinar cells that were already apparent at 6 weeks and became more extensive with age. Examination of the pancreas at 22 months of age also indicated no gross or histologic abnormalities, but electron microscopy revealed widespread degenerative changes, including dilatation of the rough endoplasmic reticulum and extensive fusion of zymogen granules affecting most of the acinar cells. Serum TLI concentration nm markedly reduced at that time, indicative of EPI, but the dog remained healthy and results of the SST were normal. Within 1 month, the dog had developed clinical signs of EPI, and not only serum Tli concentration, but also results of the N-benzoyl-L-tyrosyl-P-aminobenzoic acid test and SST were compatible with severe loss of exocrine pancreatic tissue. This loss was confirmed by gross and histologic examination of the pancreas at 25 months, which revealed typical features of pancreatic acinar atrophy, including scattered and disorganized exocrine cells in the small remnants of pancreatic tissue. These findings indicate that in German Shepherd Dogs, pancreatic acinar atrophy may involve interference with normal intracellular processing of

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.

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.

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.

Pigs from 3 litters kept under gnotobiotic conditions were inoculated orally with virulent transmissible gastroenteritis (TGE) virus, a TGE vaccine, or Hank's balanced salt solution at 2 days of age and then euthanatized at intervals ranging from 1 to 7 days after inoculation. Pigs exposed to the vaccine had clinical evidence of diarrhea and weakness. Lesions resembling those of TGE were revealed grossly, microscopically, and by scanning electron microscopy. Viral antigen was seen in intestinal epithelial cells by the direct fluorescent antibody technique. The disease induced by the vaccine virus had a longer incubation period and lesions were less severe than that induced by the virulent virus.