Development of Presumptive Sialadenosis Following a Chronic Oropharyngeal Stick Injury in a Dog.

A 3 yr old female spayed Labrador retriever was referred for the treatment of a chronic oropharyngeal stick injury. After computed tomography scan evaluation, the cervical area was explored surgically and a right-sided cervical abscess that contained a wooden stick was identified adjacent to the vagosympathetic trunk and carotid artery. The ipsilateral mandibular salivary gland was resected concurrently given its abnormal appearance, and histology confirmed inflammation and necrosis of the gland, which was suspected to be due to direct trauma from the foreign body. The clinical signs initially improved but then recurred, and a follow-up computed tomography scan was suggestive of sialadenosis or sialadenitis in the right parotid, zygomatic, and molar salivary glands. A presumptive diagnosis of sialadenosis was made and a course of phenobarbital was initiated. The clinical signs resolved completely within a few days, and there was no recurrence several months after termination of the phenobarbital treatment. This is the first case report of presumptive sialadenosis in a dog as a suspected complication of an oropharyngeal stick injury. Informed consent was obtained from the owner of the dog and the patient was managed according to contemporary standards of care.

Cricopharyngeal dysphagia and phenobarbitone-responsive sialoadenosis in a Miniature Poodle.

CASE REPORT: An 11-year-old male neutered Miniature Poodle was investigated for ptyalism, weight loss and anorexia. Cricopharyngeal dysphagia was diagnosed using fluoroscopy, and non-inflammatory salivary disease was diagnosed using a combination of cytology and computed tomography. The dog was successfully managed with phenobarbitone. CONCLUSION: To the authors' knowledge this is the first time acquired cricopharyngeal dysphagia and phenobarbitone-responsive sialoadenosis have been described together.

Septic sialoadenitis in equids: a retrospective study of 18 cases (1998-2010).

REASON FOR PERFORMING STUDY: Septic sialoadenitis, although uncommonly reported in equids, is a significant cause of pain, inappetence, dysphagia and discomfort. There are currently few reported cases possibly as a result of its infrequent occurrence. OBJECTIVES: To review cases presenting with sialoadenitis and describe the presenting complaints, results of diagnostic tests, treatment and outcome. STUDY DESIGN: Retrospective case series. METHODS: Records were reviewed for equids presenting to the UC Davis William R. Pritchard Veterinary Medical Teaching Hospital between 1998 and 2010 for salivary gland swelling. Equids were included if a diagnosis of septic sialoadenitis was made based on a combination of oral examination and/or ultrasonographic findings and/or microbial culture. Data collected included age, breed, presenting complaints, diagnostic results, treatment and outcome. RESULTS: Eighteen equids were diagnosed with septic sialoadenitis affecting the parotid gland (11) or the mandibular salivary gland (7). Ultrasound was useful to differentiate whether the mandibular or parotid salivary gland was involved. Affected equids ranged in age from 4 to 30 years (mean 17.7 years). Fourteen of 15 (93.3%) equids that underwent a complete oral examination had dental or other oral abnormalities. Six of 18 cases had evidence of sialolithiasis. Culture of the infected salivary gland or secretions was performed in 9 equids and all yielded growth of Fusobacterium sp. along with other aerobic and anaerobic bacteria. Infection resolved in 15/18 cases (83.3%) and 2/18 (11.1%) were subjected to euthanasia. CONCLUSIONS: Dental disease and sialolith formation may play important roles in the development of septic sialoadenitis in equids. Anaerobic infection should be assumed in all cases and affected horses should be treated for this until culture and sensitivity results are available. Prognosis is favourable (83.3%) with appropriate treatment.

Phenobarbital-responsive sialadenosis in dogs: case series.

Phenobarbital-responsive sialadenosis (PRS) is a rare idiopathic disease in dogs. Vomiting, retching, and gulping with bilateral enlargement of the submandibular salivary glands are the more frequent clinical signs. A thorough diagnostic examination must be performed to rule out the most important systemic etiologies involved with chronic vomiting, as there is no specific test to diagnose PRS. Diagnosis is confirmed clinically by a rapid and dramatic improvement of clinical signs after instauration of phenobarbital treatment. The aim of this article is to describe the clinical presentation, diagnostic findings, and outcome of a case series of 4 dogs with presumptive PRS.

Granulomatous giant cell submandibular sialadenitis in a dog.

A 4-month-old dog was presented with a progressive swelling of the submandibular area. The history, course, cytological, and sialographic findings were consistent with an aseptic pyogranulomatous sialadenitis with concurrent duct blockage. This rare entity, responsive to medical treatment, appears to be similar to the granulomatous giant cell sialadenitis of humans.

Sialadénite submandibulaire à cellules géantes granulomateuses chez un chien. Un chien âgé de quatre mois a été présenté avec une enflure progressive de la région submandibulaire. L'anamnèse, l'évolution, les résultats cytologiques et sialographiques étaient conformes à une sialadénite pyogranulomateuse avec un blocage concomitant des canaux.. Cette entité rare, qui a réagi au traitement médical, semble être semblable à la sialadénite à cellules géantes granulomateuses des humains.(Traduit par Isabelle Vallières).

Clinical and diagnostic imaging findings in dogs with zygomatic sialadenitis: 11 cases (1990-2009).

OBJECTIVE: To describe clinical and diagnostic imaging features of zygomatic sialadenitis in dogs. DESIGN: Retrospective case series. ANIMALS: 11 dogs with zygomatic sialadenitis and 20 control dogs without evidence of retrobulbar disease. PROCEDURES: Medical records were searched for dogs with zygomatic sialadenitis that underwent some combination of magnetic resonance imaging (MRI), computed tomography (CT), and ultrasonography. Signalment, clinical signs, results of clinicopathologic tests, cytologic and histologic diagnosis, treatment, qualitative disease features, and disease course were recorded. Images obtained via MRI or CT were analyzed for pre- and postcontrast signal intensity or density, respectively; zygomatic salivary gland area was determined. Results were compared with those of control dogs that underwent the same imaging procedures (n = 10/method). Ultrasonographic images of affected dogs were assessed qualitatively. RESULTS: Most (9/11) affected dogs were medium- or large-breed males (mean age, 8 years) with unilateral disease. Affected dogs had clinical signs of retrobulbar disease and cytologic or histologic evidence of zygomatic sialadenitis. Sialoceles were detected in 7 affected glands. Compared with values for control dogs, MRI findings in affected dogs (n = 7) included gland enlargement, T1-weighted hypointensity, T2-weighted hyperintensity, and increased contrast enhancement; CT features in affected dogs (2) included gland enlargement and hypodensity on unenhanced images. Retrobulbar masses were identified via ultrasonography in 9 of 10 orbits examined, and zygomatic salivary gland origin was detected in 4. CONCLUSIONS AND CLINICAL RELEVANCE: Visualization of anatomic structures for diagnosis of zygomatic sialadenitis and evaluation of adjacent structures was excellent via MRI and CT Ultrasonography was less definitive but useful for sample collection.

Concurrent sialocoele and necrotising sialadenitis in a dog.

A seven-year-old male, entire rottweiler was presented to Murdoch University Veterinary Hospital with a 24 hour history of blindness, chemosis, exophthalmus, pain on opening the mouth and hypersialism. Bilateral mandibular and zygomatic salivary gland enlargement with concurrent bilateral zygomatic salivary gland sialocoeles were identified. The cause of the mandibular salivary gland enlargement was confirmed as necrotising sialadenitis, while the cause of the zygomatic gland enlargement was presumed to be because of a similar disease process. No underlying aetiology was identified. Treatment consisted of supportive management, corticosteroids and paracentesis of the sialocoeles and resulted in resolution of the salivary gland enlargement and the associated clinical signs. This is an unusual presentation of salivary gland disease in the dog with multiple gland involvement and a spectrum of disease processes occurring at the same time.

Metaplastic ossification of a cervical sialocoele in a dog.

Metaplastic ossification of a long-standing cervical sialocoele was identified in a 2-year-old male Hellenic Hound dog. Diagnosis was based upon history, clinical findings, paracentesis and histopathology. Trauma or chronic inflammation of the mandibular gland/duct complex were the most probable causes of the ossification. Surgical excision of the ossified mass, as well as of mandibular and sublingual salivary glands/ducts of the affected side, resulted in clinical remission.

Idiopathic salivary gland enlargement (sialadenosis) in dogs: a microscopic study.

A histological, histochemical and morphometric study was performed on submandibular salivary glands from 13 dogs which had presented with a submandibular mass or swelling that proved to be a portion of non-inflammatory and non-neoplastic submandibular salivary gland. There were no consistent changes in lectin-binding histochemistry or immunohistochemical expression of various cell markers, and, in most cases, there was no measurable difference in acinar size in the affected gland. The possible explanation for the clinical salivary gland enlargement is therefore unclear.

Sialadenosis in dogs.

OBJECTIVE: To determine clinical findings, cytologic and histologic characteristics of salivary glands, and response to treatment with phenobarbital in dogs with clinical signs typical of sialadenosis. DESIGN: Prospective study. ANIMALS: 13 dogs with enlarged salivary glands. PROCEDURE: Data were collected from dogs with clinical signs attributable to enlarged salivary glands. Salivary gland biopsy and cytologic specimens were examined. Dogs were treated with phenobarbital and monitored for response to treatment. RESULTS: Clinical signs commonly associated with sialadenosis included retching and gulping. Substantial cellular changes were not detected by histologic or cytologic examination of enlarged salivary glands. Response to treatment with phenobarbital was rapid, although most dogs required continuous treatment to prevent recurrence of clinical signs. CONCLUSIONS AND CLINICAL RELEVANCE: Sialadenosis is a condition of unknown cause that may have been underdiagnosed in dogs. Criteria for diagnosis include typical clinical signs, enlarged salivary glands, and lack of substantial microscopic lesions. Response to treatment with phenobarbital is rapid.

IgA, IgG and IgM immunohistochemical staining in normal dog salivary glands and in cases of chronic sialadenitis.

As part of a study of normal and diseased dog salivary glands, a peroxidase-antiperoxidase immunohistochemical method was applied to study IgA, IgG and IgM staining in the major and minor salivary glands in normal dogs and in cases of sialadenitis. In normal glands, IgA was present in the plasma cells of the interlobular connective tissue and in secretory acinar epithelial cells; duct epithelium was also stained. IgG- and IgM-staining was confined to interstitial plasma cells; no epithelial staining was seen. In all glands, IgA-containing plasma cells were more numerous than those containing IgG or IgM. Larger numbers of cells containing each immunoglobulin were present in sublingual glands than in parotid, submandibular, zygomatic, palatine or tongue glands. In the submandibular glands in which there were signs of salivary gland inflammation, there were increased numbers of plasma cells containing each of the immunoglobulin isotypes but the proportion of different isotypes was unchanged.

Isolation and characterization of sialodacryoadenitis virus (coronavirus) from rats by established cell line LBC.

The outbreak of sialoadenitis occurred in a laboratory rat colony and the causative agent was isolated from the affected salivary glands of diseased rats using the established cell line LBC. The isolate readily multiplied, producing clear cytopathic effects with syncytium formation, and it was identified virologically and serologically as rat sialodacryoadenitis virus. In attempts to isolate the virus by primary rat kidney (PRK) cells and suckling mice as well as LBC cells, the LBC cells showed higher susceptibility for the virus growth as compared with PRK cells or the brain of suckling mice. The isolation rate of virus was 100% (5/5) in LBC, 40% (2/5) in PRK cells and 60% (3/5) in suckling mice. After four passages in the LBC cells, the virus did not produce disease in adult rats, while the mouse brain-passaged virus did.

Sialadenitis associated with periorbital disease in a dog.

Submucosal sialadenitis was diagnosed on histologic examination of a biopsy specimen from a palatine swelling associated with acute, unilateral periorbital disease in a dog. Sialadenitis may have been the cause of periorbital disease or may have been part of a generalized inflammatory condition affecting the periorbital tissues. Corticosteroids were immediately effective in eliminating signs of periorbital disease and sialadenitis. A 3-month corticosteroid treatment was used because the sialadenitis and periorbital disease were immune-mediated. This dog has been free of recurring signs for more than 3 years.

Salivary gland disease in dogs and cats: 245 cases (1985-1988).

Diagnostic pathology records spanning 41 months (July 1985 through November 1988) were searched for diagnoses of salivary gland disease in dogs and cats. Review of 87,392 records from that period revealed 245 cases (0.3%) in which salivary gland tissue had been evaluated. During that period, salivary gland tissue was submitted to the laboratory almost twice as often from dogs (160 cases) as from cats (85 cases). On the basis of histologic examination, 89% of salivary gland submissions from small animal practices were allotted to 1 of 5 major categories: malignant neoplasms (30%; 74/245), sialadenitis (26%; 64/245), normal salivary gland (16%; 40/245), sialocele (9%; 21/245), and salivary gland infarction (8%; 20/245). The remaining 11% of submissions included various degenerative or fibrotic lesions, ductal ectasia, sialolithiasis, edema, benign neoplasia, and secondary salivary involvement with systemic or cervical lymphosarcoma or with fibrosarcoma in the head and neck.

Coronavirus infection in the laboratory rat: immunization trials using attenuated virus replicated in L-2 cells.

Sixty-nine specific pathogen-free male Wistar rats approximately eight weeks of age were used to evaluate the efficacy of an attentuated strain of sialodacryoadenitis (SDA) virus in providing protection against infection on subsequent challenge with virulent SDA virus. Fifty-four animals were inoculated intranasally with approximately 10(3.5) median cell culture infectious doses of the 25th passage of SDA virus in L-2 cells. Randomly-selected vaccinated animals were killed in order to evaluate the safety and efficacy of attenuated virus by histopathological examination of the salivary glands, lacrimal glands, and lower respiratory tract, and titration of sera for antibody to SDA virus. At three months and six months postvaccination (pv), animals were selected at random and challenged with virulent SDA virus. Seronegative, age-matched animals were also challenged, and served as controls. In animals examined at six to ten days pv, lesions were absent in submandibular and parotid salivary glands and lacrimal glands, but transient lesions were present in major airways of the lower respiratory tract. In a comparison of the incidence and extent of lesions, and antibody titers in challenged vaccinates and seronegative controls, lesions were minimal or absent in vaccinates compared to challenged naive rats, particularly in animals inoculated at three months pv. In addition, antibody titers in challenged vaccinates were much higher than were postinoculation titers in inoculated controls. In a comparison of lesions in salivary and lacrimal glands in vaccinated and control animals challenged at six months pv, there was a significant reduction in the number of animals without lesions in the vaccinated group (p = less than 0.0001).(ABSTRACT TRUNCATED AT 250 WORDS)

Sialodacryoadenitis in the rat: effects of immunosuppression on the course of the disease.

Eight-week-old outbred male and female Crl:CD(SD)BR rats were treated with prednisolone (PR) or cyclophosphamide (CY) and were inoculated intranasally with sialodacryoadenitis (SDA) virus. The course of the disease was compared with nonimmunosuppressed, SDA virus-inoculated rats of the same stock. Criteria used to compare SDA in the 3 groups, included histologic changes in salivary and lacrimal glands, immunofluorescent microscopy of paraffin-embedded tissues, serum amylase levels, and antibody response. Based on these criteria, there was little detectable difference in the course and intensity of SDA in PR-treated and nonimmunosuppressed rats. In CY-treated rats, there was a delay in the onset of SDA, in the appearance of inflammatory cells in affected glands, and in the reparative process in the salivary and lacrimal glands. Viral antigen persisted longer in CY-treated rats than in PR-treated and nonimmunosuppressed rats. Antibody to SDA virus was not detected in CY-treated rats. The efficacy of immunosuppression by PR and CY was confirmed by the sheep erythrocyte agglutination procedure performed in selected rats. Male and female rats of the same strain were immunosuppressed beginning 4 weeks after inoculation with SDA virus to produce recrudescence of the disease. Histologic examination of salivary and lacrimal glands, immunofluorescent microscopy, serum amylase values, and viral isolation studies did not reveal evidence of reactivation of a persistent viral infection or viral shedding. Based on these studies, there is no evidence that SDA virus may persist as an inapparent infection after recovery from the disease.

Comparison of strain susceptibility to experimental sialodacryoadenitis in rats.

Wistar, Sprague-Dawley, and Long-Evans outbred rats, and the Fischer344 inbred strain were inoculated intranasally with 10(3) TCID50 of sialodacryoadenitis virus at approximately 9 weeks of age. Paired animals were killed at 2-day intervals post inoculation up to 2 weeks, then at 20 days. A comparison of strain susceptibility to sialodacryoadenitis virus was made using the following criteria: histopathology, immunofluorescent microscopy, serology and serum amylase activity. All four strains were susceptible to sialodacryoadenitis virus. The disease was frequently subclinical, although typical lesions were observed on histopathology. Focal bronchitis, bronchiolitis and pneumonitis were observed histologically during the acute stages of the disease. Immunohistochemistry was performed on trypsin-treated, paraffin-embedded sections, and viral antigen was readily demonstrated in salivary and lacrimal glands during the early stages of the disease. A rise in serum amylase was observed, and it was correlated with the first appearance of lesions in the salivary glands. Based on serology and immunofluorescence microscopy, the appearance of detectable antibody to sialodacryoadenitis virus, and the rate of viral clearance from infected glands, the course of the disease was similar in the four strains studied.

Papovaviral sialoadenitis in athymic nude rats.

A wasting disease was found in 32 athymic nude rats. The rats had parotid sialoadenitis with intranuclear inclusion bodies in ductal and acinar epithelial cells. Other common lesions included bronchitis, bronchiolitis and secondary bacterial pneumonia. Less commonly, rhinitis and Harderian adenitis were seen. Intranuclear inclusions were also seen in bronchial epithelium of 1 rat, Harderian gland acini of 1 rat and laryngeal glands of 2 rats. Viral particles, averaging 45 nm in diameter, sometimes in crystalline arrays, were found in the nucleus of parotid epithelial cells. By the use of the avidin-biotin-peroxidase complex (ABC) immunoperoxidase technique, antibodies to disrupted SV40 virus (the group specific antigen of the polyomavirus (miopapovavirus) genus of the papovavirus family) reacted with intranuclear inclusions and cytoplasm of parotid epithelium and inclusions in lung and Harderian gland. The viral antigen did not cross react with antibodies to mouse polyoma, mouse K or disrupted bovine papilloma viruses.

A subclinical epizootic of sialodacryoadenitis in rats.

An epizootic of sialodacryoadenitis was identified in 10-week-old rats 5 days after they were housed with a group of older rats. The young rats generally did not develop the characteristic clinical signs of sialodacryoadenitis, but they did have typical histologic lesions of sialodacryoadenitis in Harderian, lacrimal, and salivary glands. The lesions were variable in distribution and severity, and chronic lesions persisted in the Harderian glands of the rats.