A retrospective study of the clinical, histological, and immunohistochemical manifestations of 5 dogs originally diagnosed histologically as necrotizing scleritis

Purpose To describe the clinical, histological, and immunohistochemical manifestations of canine necrotizing scleritis. Methods A retrospective examination of the clinical records and samples of ocular tissues from five dogs with a histological diagnosis ‘necrotizing scleritis’ was completed. Archived, formalin‐fixed, paraffin‐embedded samples and two control globes were stained with hematoxylin and eosin, Gram, periodic acid–Schiff (PAS) and Masson trichrome stains, and they were immunohistochemically labeled for CD3, CD18, and CD20. Results Of the five cases reviewed, only two could be confirmed as idiopathic necrotizing scleritis. The other three cases were retrospectively diagnosed as unilateral focal, non‐necrotizing scleritis, one as episcleritis and the third was scleritis secondary to a proptosed globe based on our retrospective clinical, histological, and immunohistochemical evaluations. In these two cases, idiopathic necrotizing scleritis manifested as a bilateral, progressive, inflammatory disease of the sclera and cornea that induces significant uveitis. Light microscopic examination confirmed collagen degeneration and granulomatous inflammation. There was no evidence for an infectious etiology based on Gram’s and PAS stainings. Immunohistochemical labeling revealed a predominance of B cells in idiopathic, bilateral necrotizing scleritis. Tinctorial staining abnormalities with Masson’s trichrome stain were present in scleral collagen of the two cases with idiopathic necrotizing scleritis as well as a case of secondary traumatic scleritis. Conclusions Based on a limited number of cases, idiopathic canine necrotizing scleritis shares similar histopathological features with non‐necrotizing scleritis and episcleritis; however, necrotizing scleritis is B‐cell‐dominated and bilateral, and significant collagen alterations manifest with Masson’s trichrome stain.     

Experimental Use of Fluoroalkyl Cyanoacrylate in Canine Urethral Anastomosis

The results of a study designed to evaluate a fluoroalkyl cyanoacrylate tissue adhesive as an adjunct to suture anastomosis of the severed canine pelvic urethra are presented. The urethral anastomotic sites were evaluated by contrast radiography, gross pathology, and histopathology. Urethral anastomosis resulted in a clinically functional urethra in all 6 control dogs (suture anastomosis) and 5 of the 6 test dogs (suture anastomosis plus adhesive). A severe stricture at the anastomotic site developed in 1 dog in the test group. Evidence of leakage was detected by contrast radiography in 1 dog of each group. Microscopic evidence of incomplete closure was detected in 4 control dogs and 2 test dogs. An extensive granulomatous inflammatory reaction was associated with use of the adhesive. The lower incidence of microscopic leakage observed in the test dogs was attributed to fibroplasia induced by the cyanoacrylate and not to the adhesive properties of the cyanoacrylate.     

Transarterial ductal occlusion with the Amplatzer vascular plug in 31 dogs

Background: Transarterial ductal occlusion with the Amplatzer vascular plug was first reported in dogs by Hogan et al in 2005. Hypothesis: Use of the Amplatzer vascular plug is a safe, efficacious method of patent ductus arteriosus (PDA) occlusion. Animals: Thirty‐one client‐owned dogs with PDA. Methods: Records of 31 dogs in which transarterial occlusion of PDA with an Amplatzer vascular plug was attempted were reviewed. Results: All dogs had a type II PDA, with 27 dogs having type IIA morphology and 4 dogs having type IIB morphology. Appropriate device deployment was achieved in 29 of 31 dogs. Postdeployment angiography in 21 dogs documented complete occlusion in 10 dogs, trivial residual flow in 5 dogs, mild residual flow in 2 dogs, moderate residual flow in 3 dogs, and severe residual flow in 1 dog. Transthoracic color Doppler echocardiography documented complete occlusion in 22 dogs, whereas 2 dogs had trivial residual flow, 2 dogs had mild residual flow, 2 dogs had mild to moderate residual flow, and 1 dog had severe residual flow. Of the 7 dogs with residual flow, 2 had complete occlusion 2–4 months postoperatively, 1 had moderate residual flow 1 month postoperatively, and 4 were lost to follow‐up. One dog required a larger device than was able to be deployed through the largest sheath placed in the femoral artery. Pulmonary embolization of the device occurred in 1 dog. Conclusion: We conclude that ductal occlusion with an Amplatzer vascular plug is a safe and efficacious therapy for PDA in dogs.     

Fatal mycobacteriosis with hepatosplenomegaly in a young dog due to Mycobacterium avium.

Cases of disseminated Mycobacterium avium infections in dogs are rare because it appears that the species is innately resistant to infection. A 2-year-old, castrated, 5 kg Shih Tzu-Poodle-cross developed anemia, abdominal pain, lethargy, and splenomegaly. Histological examination of surgically removed spleen indicated marked granulomatous splenitis with myriad intracytoplasmic acid-fast bacterial rods. Ultrastructural examination revealed the presence of 3-4-microm-long mycobacteria in phagolysosomes of epithelioid macrophages. Tissue extract of lightly fixed spleen was positive for M. avium 16S ribosomal RNA and negative for M. tuberculosis complex IS6110 DNA by polymerase chain reaction testing. Anemia was associated with the presence of mycobacteria-infected macrophages in bone marrow. The animal's condition deteriorated, and euthanasia was performed after a clinical course of 2 months. The principal morphological findings at necropsy were severe diffuse granulomatous hepatitis, enteric lymphadenomegaly, and segmental granulomatous enteritis with intralesional mycobacteria present. Mycobacterium avium was cultured from enteric lymph nodes sampled at necropsy. The source of infection was not established but was presumed to be environmental with an enteric portal of entry.     

CONTRAST‐ENHANCED PORTAL MAGNETIC RESONANCE ANGIOGRAPHY IN DOGS WITH SUSPECTED CONGENITAL PORTAL VASCULAR ANOMALIES

Contrast‐enhanced multiphase magnetic resonance angiography (CE‐MRA) was used in 17 dogs with a suspected congenital portal vascular anomaly. Portal vascular anomalies were identified in 16 of the 17 dogs. Eleven had a single intrahepatic portocaval shunt (two central divisional, three right divisional, and six left divisional), one dog had a double intrahepatic portocaval shunt, one dog had a hepatic arteriovenous malformation, one dog had a complex intrahepatic porto‐caval shunt. Two dogs had an extrahepatic portosystemic shunt and no shunt was identified in one dog. Total imaging time was <10 min and image quality was good to excellent in all dogs. Portal CE‐MRA is a feasible, fast and non invasive technique to diagnose portal vascular anomalies in dogs, with a large field‐of‐view and good anatomic depiction of the abnormal vessels. Based on these results, CE‐MRA is an efficient imaging technique for the diagnosis of portal vascular anomalies in dogs.     

Expression of vascular endothelial growth factor in tumors and plasma from dogs with primary intracranial neoplasms

OBJECTIVE: To quantitatively evaluate expression of vascular endothelial growth factor (VEGF) in intracranial tumors in dogs and determine whether relationships exist between circulating and intratumoral VEGF concentrations and tumor type and grade. ANIMALS: 27 dogs with primary intracranial neoplasms and 4 unaffected control dogs. PROCEDURES: Plasma and brain tumor samples were obtained from each dog, and plasma and intratumoral concentrations of VEGF were measured by use of an ELISA. RESULTS: Dogs with meningiomas (n = 11) were significantly older than dogs with oligodendrogliomas (7) or astrocytomas (9). Measurable VEGF was detected in all tumors, and a significant negative correlation between age and intratumoral VEGF concentration was detected. Age-adjusted comparisons identified significant differences in intratumoral VEGF concentrations among all tumor types; the highest VEGF concentrations were associated with astrocytomas. Within each tumor type, increasing tumor grade was significantly associated with increasing VEGF expression. Plasma VEGF concentrations were detectable in 9 of 27 dogs; the proportion of dogs with astrocytomas and a detectable circulating VEGF concentration (7/9 dogs) was significantly higher than the proportion of dogs with meningiomas (1/11 dogs) or oligodendrogliomas (1/7 dogs) with a detectable circulating VEGF concentration. CONCLUSIONS AND CLINICAL RELEVANCE: Overexpression of VEGF appears common in canine astrocytomas, oligodendrogliomas, and meningiomas. In the neoplasms examined, intratumoral VEGF concentrations correlated well with tumor malignancy. The VEGF expression patterns paralleled those of analogous human tumors, providing evidence that dogs are a suitable species in which to study angiogenesis and intracranial neoplasia for human application.     

Nodular granulomatous episclerokeratitis in dogs: 19 cases (1973-1985)

We examined the age and breed prevalence and the response to treatment of 19 dogs with nodular granulomatous episclerokeratitis. Biopsy specimens were evaluated to determine the histologic characteristics of the lesions. In these dogs, this disorder was an idiopathic, bilateral disease characterized histologically by the presence of chronic granulomatous inflammation and reticulin fiber formation. The onset of clinical signs developed predominantly in young to middle-aged Collies, with a slow progression and benign clinical course. With treatment, the condition rarely threatened vision and was controlled easily with azathioprine (2 mg/kg) and/or corticosteroid. The dose of immunosuppressive drug was tapered to allow for minimal systemic effects and continued remission of clinical signs. The response to treatment was highly variable.     

Juvenile sterile granulomatous dermatitis and lymphadenitis in the dog

Juvenile sterile granulomatous dermatitis and lymphadenitis is a rare immune-mediated skin disease in young dogs. History, signalment, diagnostics, treatment, and outcome in 10 dogs are described. The age ranged from 8 - 36 weeks. The lymph nodes were enlarged in all dogs, especially the mandibular and prescapular lymph nodes. Systemic signs including fever were present in 8 dogs. Seven dogs suffered from blepharitis and painful edema of the muzzle with hemorrhagic discharge, pustules and papules. Cytology of pustules and lymph node aspirates revealed a pyogranulomatous inflammation. In 7 cases the diagnosis of juvenile sterile granulomatous dermatitis and lymphadenitis was confirmed by histology. Nine dogs were treated with prednisolone (0.5 - 1.25 mg/kg BID), H2-receptor antagonists and analgetics; all dogs were treated with antibiotics. Four dogs were treated with eye ointment containing antibiotics and glucocorticoids. The prednisolone dosage was tapered over 3 - 8 weeks. One dog had a relapse.     

Use of cyclosporine to treat granulomatous meningoencephalitis in three dogs

Use of cyclosporine to treat granulomatous meningoencephalitis in three dogs Three dogs with a presumptive diagnosis of granulomatous meningoencephalitis were treated with orally administered cyclosporine. In 2 dogs, cyclosporine administration replaced initial corticosteroid administration, and in 1 dog, cyclosporine was the only treatment used. One dog had the focal form of the disease in the brainstem, 1 dog had the focal form in the forebrain associated with a concurrent ocular form, and 1 dog had the disseminated form of disease. At 12-month follow-up, the 2 dogs with the focal form of the disease had no clinical signs. The dog with the disseminated form improved only partially, and euthanasia was performed 3 weeks after initial evaluation. Cyclosporine was considered effective at an initial dosage of 6 mg/kg (2.7 mg/lb) every 12 hours. Adverse effects associated with cyclosporine administration included transient lymphopenia, excessive shedding, and focal symmetric hair discoloration.     

Attempts to produce granulomatous colitis in Boxer dogs with a mycoplasma.

Four of six Boxer dogs with granulomatous colitis had mycoplasmas in the colon and three in the draining lymph node as well. One isolate identical with Mycoplasma strain HRC-689 was inoculated into the colon of five Boxer dogs at eight weeks of age; four controls were inoculated with medium. Animals were killed at two week intervals and examined. The mycoplasma strain produced changes of the colon characterized by lymphocytic infiltration of mucosa, lymphocytic submucosal perivasculitis, and enlargement of colonic lymphoid nodules but granulomatous colitis did not occur. The experimental dogs developed antibodies, and dogs from a kennel with a high prevalence of colitis cases had high antibody titers against strain HRC-689.     

Hypercalcaemia associated with granulomatous lymphadenitis and elevated 1,25 dihydroxyvitamin D concentration in a dog

A seven-year-old Labrador was presented with weight loss and mild generalised lymphadenopathy. Histopathology of an excised lymph node by the referring veterinarian demonstrated granulomatous lymphadenitis. At the time of referral, fine-needle aspirates of the lymph nodes confirmed the presence of ongoing granulomatous inflammation. Further investigations revealed marked hypercalcaemia, a low parathyroid hormone concentration, a parathyroid hormone related protein concentration within the reference range, and an elevated serum concentration of 1,25 dihydroxyvitamin D. An underlying cause of the granulomatous lymphadenitis could not be identified. The clinical signs, hypercalcaemia and elevated serum concentrations of 1,25 dihydroxyvitamin D resolved following prednisolone treatment. In contrast to dogs, hypercalcaemia occurred secondarily to granulomatous disease and elevated 1,25 dihydroxyvitamin D concentrations is a well-recognised condition in human beings. To the authors' knowledge, this is the first case report to describe elevated serum calcium and 1,25 dihydroxyvitamin D concentrations in a dog with histologically confirmed granulomatous disease.     

Retrospective evaluation of potential causes associated with clinically relevant hyperlactatemia in dogs with lymphoma

The aim of this study was to determine whether or not canine lymphoma could be associated with a clinically relevant type B hyperlactatemia (> 2.5 mmol/L). The medical database from the University of Montreal Veterinary Medical Teaching Hospital was searched for confirmed cases of canine lymphoma with a blood lactate measurement. Information retrieved included stage, clinical observations compatible with causes of type A and B hyperlactatemia other than cancer, hepatic involvement, and drugs administered. Twenty (40%) dogs were hyperlactatemic. Five dogs (10%) were classified as having cancer-related hyperlactatemia. Seventy-five percent of hyperlactatemic dogs had clinical evidence of type A hyperlactatemia. In addition to lymphoma, 70% of hyperlactatemic dogs had evidence of an additional cause of type B hyperlactatemia. A significant association (P = 0.01) was identified between corticosteroid administration and hyperlactatemia. Cytological, echographic, and/or biochemical tests revealed hepatic changes in all hyperlactatemic dogs. Lymphoma alone may not be sufficient to explain clinically relevant hyperlactatemia in dogs.     

Characterization of interstitial nephritis in pigs with naturally occurring postweaning multisystemic wasting syndrome

Kidney samples with interstitial nephritis from 26 pigs affected by postweaning multisystemic wasting syndrome (PMWS) were selected. A histologic evaluation was carried out to describe the type of inflammation and its relationship with viral load, as assessed by in situ hybridization (ISH). Of 26 cases, 10 revealed a tubulointerstitial, lymphoplasmacytic nephritis, 11 an interstitial granulomatous nephritis, and 5 both types of inflammation (mixed type). In 4 cases of granulomatous inflammation, the pattern was not classically nodular, and a population of macrophages and lymphocytes was present (interstitial lymphohistiocytic nephritis). ISH confirmed the presence of porcine circovirus type 2 (PCV2) nucleic acid in all cases. The epithelium of the renal tubules was the most constantly ISH-positive structure. In tubulointerstitial nephritis, the higher the number of positive inflammatory cells, the more severe the inflammation. The ISH reaction was more heterogeneous and unpredictable in granulomatous nephritis, with some epithelioid and giant cells positive by ISH. To quantify macrophages distributed in the three patterns of nephritis, immunohistochemical methods using anti-major histocompatibility complex II (anti-MHC-II) and anti-lysozyme antibodies were undertaken, and semiquantitative evaluation was carried out. MHC-II was mainly expressed by lymphocytes in tubulointerstitial nephritis, but did not always stain macrophages in cases of granulomatous (including lymphohistiocytic) nephritis; the anti-lysozyme antibody revealed macrophages when present in tissues. The amount of PCV2 nucleic acid was not apparently associated with the pattern of inflammation (tubulointerstitial or granulomatous). PCV2 load seems to reflect the severity of the lymphoplasmacytic inflammation but not that of granulomatous and lympho histiocytic types.     

Histopathologic features of canine heartworm microfilarial infection after treatment with ivermectin

Tissues of dogs treated with ivermectin were examined microscopically to learn the fate of microfilariae of canine heartworm that disappear from the peripheral circulation within a few days of treatment. Medicated dogs were killed 18 hours, 3 days, and 6 days after treatment with 0.5 mg of ivermectin/kg of body weight subcutaneously. Ivermectin was dissolved in 60% propylene glycol and 40% glycerol formal. In dogs killed at posttreatment hour 18, the peripheral microfilaremia had decreased by an average of 89%. At this time, a dense mass of RBC, WBC, and macrophages plus many microfilariae was found in pulmonary alveolar septae. Similar reactions were seen in liver, kidney, and spleen. Phagocytosis of microfilarial fragments was evident. In dogs killed at posttreatment day 3, many microfilariae were fragmented and phagocytosis of the fragments was common. In dogs killed at posttreatment day 6, microgranulomas were common, particularly in such vascular organs as lungs, kidney, and liver. Microgranulomas containing microfilariae were also seen in spleen, skeletal and cardiac muscles, diaphragm, lymph nodes, gastrointestinal tract, and pancreas. Small glial nodules were seen in the CNS. Denudation of the atrial epicardium was associated with fragments of microfilariae and granulomatous inflammatory cells. Renal epithelial crescents were observed in treated and nontreated dogs. Plasma cells were conspicuous in treated and nontreated dogs, especially in some livers and kidneys. Before treatment, all dogs were severely microfilaremic. At the end of the experiment, the peripheral microfilaremia was reduced by 98%.(ABSTRACT TRUNCATED AT 250 WORDS)     

The histological appearance of peroral gastric biopsies in clinically healthy and vomiting dogs.

A survey of the histology of gastric biopsies in 501 dogs, consisting of 19 clinically healthy dogs and 482 vomiting dogs is presented. Whole stomachs of four young clinically healthy laboratory dogs were used as controls. Eleven percent of forceps biopsies were unsuitable for examination; all suction biopsies were of good quality. Slight to severe gastritis was found in 168 vomiting dogs (35%), whereas five dogs (26%) of the clinically healthy group showed a mainly slight gastritis. Superficial and diffuse gastritis were the most prominent findings in the 168 dogs with gastritis. A single type of gastritis was found in 114 dogs, a combination of different types in 54 dogs. Gastric atrophy was seen in 23 (5%) vomiting dogs and in three (15%) clinically healthy dogs, atrophy with a slight to severe fibrosis in 21 (4%) vomiting dogs, and in 84 (17%) vomiting dogs and two (11%) healthy dogs, gastric fibrosis was present. Carcinomas were seen in 26 vomiting dogs, of which 17 also had gastritis. A differential diagnosis of granulomatous gastritis/carcinoma had to be made in one case. Seven dogs showed a lymphosarcoma, and in six other dogs a differential diagnosis of lymphosarcoma and/or gastritis was made. One adenomatous polyp was seen. In one clinically healthy dog an adenomyoma was diagnosed. Ulceration was found in 24 dogs, but only five of these lacked other lesions. Other biopsy findings were pseudopyloric metaplasia, hyperplasia, cysts, calcification and edema. Some dogs showed "antralization".     

Morphologic features and development of granulomatous vasculitis in feline infectious peritonitis

Feline infectious peritonitis (FIP) is a fatal, coronavirus (CoV)-induced systemic disease in cats, characterized by granulomas in organs and granulomatous vasculitis. This study describes the morphologic features of granulomatous vasculitis in FIP as well as its development in the course of monocyte-associated feline CoV (FCoV) viremia in five naturally infected Domestic Shorthair cats with FIP. Monocyte-associated FCoV viremia was demonstrated by immunohistology, RNA in situ hybridization, and electron micropscopy. Granulomatous phlebitis at different stages of development was observed. Vasculitic processes ranged from attachment and emigration of FCoV-infected monocytes to vascular/perivascular granulomatous infiltrates with destruction of the vascular basal lamina. Monocytes as well as perivascular macrophages were activated because they were strongly positive for CD18 and expressed cytokines (tumor necrosis factor-alpha and interleukin-1beta) and matrix metalloproteinase-9. In addition, general activation of endothelial cells, represented by major histocompatibility complex II upregulation, was observed in all cases. These results confirm FIP as a monocyte-triggered systemic disease and demonstrate the central role of activated monocytes in FIP vasculitis.     

Effect of acetylsalicylic acid on vascular damage and myointimal proliferation in canine pulmonary arteries subjected to chronic injury by Dirofilaria immitis

The effect of aspirin (ASA) on pulmonary artery response to chronic injury induced by Dirofilaria immitis was assessed in the dog. Eight dogs were studied for 30 days after adult heartworms were transplanted into the pulmonary arteries. Four dogs were treated with ASA (325 mg/day given orally) starting 3 days before the transplantation was done. Evan's blue dye was used to locate areas of vascular damage. Vascular morphology was assessed by scanning electron microscopy and light microscopy. According to results of the morphologic studies, nontreated dogs had extensive endothelial damage and significant adhesion of leukocytes and blood platelets. Blood vessels of ASA-treated dogs had less endothelial damage. Platelet adhesion on areas of vascular damage was less than that observed in nontreated dogs. Myointimal proliferative lesions were observed in both nontreated and ASA-treated dogs. However, the lesions in nontreated dogs were larger (means 68 +/- 7 mm2) and more complex than those in ASA-treated dogs (means 20 +/- 1 mm2). The results indicated that aspirin may protect against development of myointimal proliferation resulting from chronic vascular injury. The mechanism of the ASA protection may result from a combination of antiplatelet and anti-inflammatory effects, as well as a direct protective effect on vascular endothelium.     

Pythiosis of the digestive tract in dogs from Oklahoma

Enteric pythiosis was diagnosed in nine dogs in Oklahoma. Eight dogs had anorexia and weight loss. Two of these dogs had diarrhea; two dogs exhibited vomiting and diarrhea; and one dog had vomiting. One dog presented with dysphagia. Seven dogs had either a palpable or radiographically visible abdominal mass. These seven dogs had localized regions of mucosal ulceration and thickened gastric or intestinal walls with some involvement of the adjacent mesentery or omentum. Two dogs had enlarged regional mesenteric lymph nodes. One dog that presented with dysphagia had an oropharyngeal mass involving the larynx and cranial esophagus. Microscopically, there was transmural chronic sclerosing and granulomatous to pyogranulomatous inflammation with arteritis. Pythium spp. were identified in all specimens by immunohistochemistry.     

Unusual vascular ring anomaly associated with a persistent right aortic arch in two dogs

An unusual vascular ring anomaly consisting of a persistent right aortic arch and a left ligamentum arteriosum extending from the main pulmonary artery to an aberrant left subclavian artery and left aortic arch remnant complex was identified in a German shepherd dog and a great Dane. The left subclavian artery and left aortic arch remnant complex originated at the junction between the right distal aortic arch and the descending aorta and coursed dorsal to the oesophagus in a cranial direction. The attachment of the ligamentum arteriosum to the aberrant left subclavian artery was approximately 5 cm cranial to the point of origin of the aberrant left subclavian artery and left aortic arch remnant complex from the descending aorta in both dogs. This anomaly observed in both dogs is similar to an anomaly reported in humans, in which a persistent right aortic arch is found in conjunction with an aberrant left subclavian artery and a left aortic arch remnant (Kommerell's diverticulum). Surgical ligation and division of the left ligamentum arteriosum in both dogs, along with division of the left subclavian artery in the great Dane, resulted in resolution of clinical signs in both of the dogs in this report.     

Immunohistochemical demonstration of canine distemper virus antigen as an aid in the diagnosis of canine distemper encephalomyelitis

Brain tissue from 33 dogs with non-suppurative encephalitis was examined for evidence of canine distemper virus (CDV) encephalitis. Sections were examined for lesions, inclusion bodies, syncytial cells and CDV antigen using a double bridge unlabelled antibody enzyme technique. Histopathological lesions considered to be typical of granulomatous meningoencephalomyelitis were found in seven dogs. They all lacked inclusion bodies, syncytial cells and CDV antigen. The remaining 26 dogs all had histopathological lesions typical of CDV encephalitis. Inclusion bodies were found in 24 dogs, four of which also had syncytial cells and CDV antigen was detected immunocytochemically in 25. One dog had no inclusion bodies or syncytial cells and was immunohistochemically negative. Syncytial cells have been found to be of limited diagnostic value for the diagnosis of CDV encephalitis. While inclusion bodies proved to be a good diagnostic criterion for the confirmation of CDV infection, the immunohistochemical demonstration of CDV antigen proved to be superior. CDV antigen was more prevalent than inclusion bodies in tissue sections and much more easily detectable.