Clinical manifestations of chronic pancreatitis in English cocker spaniels.

BACKGROUND: Chronic pancreatitis (CP) is common in English cocker spaniels (ECS). It is histologically similar to IgG4-related disease (IgG4-RD) in humans and is characterized by duct destruction, interlobular fibrosis, and dense periductular and perivenous lymphocytic aggregates. However, the clinical manifestations of CP in ECS have not been previously described. OBJECTIVES: Characterize the clinical manifestations of CP in a group of ECS, including similarities and differences to IgG4-RD in humans. ANIMALS: One-hundred four ECS with CP and 44 client owned control ECS without CP (both healthy and diseased controls). METHODS: Affected dogs were divided into 2 groups according to the methods used to diagnose CP. Case records were searched for signalment, clinical, and clinicopathological findings, and evidence of keratoconjunctivitis sicca (KCS), proteinuria, other immune-mediated diseases, and anal sacculitis. RESULTS: Involvement of other organs was common. Affected ECS presented with a high frequency of KCS (n = 49), proteinuria (n = 47), anal gland disease (n = 36), atopy (n = 21), and other immune-mediated diseases (n = 16). Those with parti-color hair coats, particularly blue roan, had a strong association with CP, suggesting a link between coat color and autoimmune conditions in this breed. CONCLUSIONS AND CLINICAL IMPORTANCE: English cocker spaniels with CP show clinical similarities to humans with IgG4-RD and common involvement of other organs. Clinicians should evaluate affected Cocker Spaniels for proteinuria, keratoconjunctivitis sicca, and other potential immune-mediated diseases.

Candidate circulating microRNA biomarkers in dogs with chronic pancreatitis.

BACKGROUND: Pancreatitis is an important cause of disease and death in dogs. Available circulating biomarkers are not sufficiently sensitive and specific for a definitive diagnosis. HYPOTHESIS: Circulating microRNAs would be differentially expressed in dogs with chronic pancreatitis and could have potential as diagnostic biomarkers. ANIMALS: Healthy controls (n = 19) and dogs with naturally occurring pancreatitis (n = 17). METHODS: A retrospective case-control study. Dogs with pancreatitis were included if they satisfied diagnostic criteria for pancreatitis as adjudicated by 3 experts. MicroRNA was extracted from stored serum samples and sequenced. Reads were mapped to mature microRNA sequences in the canine, mouse, and human genomes. Differentially expressed microRNAs were identified and the potential mechanistic relevance explored using Qiagen Ingenuity Pathway Analysis (IPA). RESULTS: Reads mapping to 196 mature microRNA sequences were detected. Eight circulating microRNAs were significantly differentially expressed in dogs with pancreatitis (≥2-fold change and false discovery rate <0.05). Four of these mapped to the canine genome (cfa-miR-221, cfa-miR-222, cfa-miR-23a, and cfa-miR-205). Three mapped to the murine genome (mmu-miR-484, mmu-miR-6240, mmu-miR-101a-3p) and 1 to the human genome (hsa-miR-1290). Expression in dogs with pancreatitis was higher for 7 microRNAs and lower for mmu-miR-101a-3p. Qiagen IPA demonstrated a number of the differently expressed microRNAs are involved in a common pancreatic inflammatory pathway. CONCLUSIONS: The significantly differentially expressed microRNAs represent promising candidates for further validation as diagnostic biomarkers for canine pancreatitis.

Utility of 1,2-o-dilauryl-rac-glycero glutaric acid-(6'-methylresorufin)-ester-lipase for monitoring dogs with chronic pancreatitis.

BACKGROUND: The utility of 1,2-o-dilauryl-rac-glycero glutaric acid-(6'-methylresorufin)-ester-(DGGR)-lipase activity (DLA) in monitoring clinical progression of chronic pancreatitis (CP) in dogs is unknown. OBJECTIVE: To examine the association of DLA with clinical signs of CP, as assessed by a CP clinical severity score (CPCSS). ANIMALS: Twenty-four dogs. METHODS: This is a retrospective study. Chronic pancreatitis was diagnosed based on clinical signs and DLA > 250 U/L and monitored using CPCSS and DLA. RESULTS: The study included 134 visits (median, 10 visits/dog; range, 2-11). Mild-moderate (CPCSS, 0-3) and severe (CPCSS, ≥4) disease were documented in 94 (70%) and 40 (30%) visits, respectively. In emergency visits (n = 44; 33%) CPCSS (median, 5; range, 0-15) and DLA (median, 534 U/L; range, 63-7133) were higher (P < .001 and P = .003, respectively) than in scheduled ones (n = 90; 67%; median, 1; range, 0-6 and median, 384 U/L; range, 49-3747, respectively). DGGR-lipase activity was associated (P = .009) with the CPCSS, with a lower activity documented in mild-moderate CPCSS (median 391 U/L; range, 49-3747), compared to severe score (median, 558 U/L; range, 63-7133). DGGR-lipase activity was significantly, but weakly, correlated with CPSS (r = 0.233, P = .007). DGGR-lipase activity inefficiently discriminated mild-moderate vs severe CP (area under the receiver operator characteristics curve, 0.64; 95% confidence interval, 0.53-0.75; P = .012), with DLA cutoff of 428 U/L corresponding to sensitivity of 65% and specificity of 63%. CONCLUSIONS AND CLINICAL IMPORTANCE: Increased DLA is associated with emergency revisits in dogs with CP, possibly reflecting acute flare-ups. DGGR-lipase activity was associated with the CPCSS over the follow-ups but could not differentiate disease severity.

Neural Hypertrophy and Hyperplasia in a Case of Chronic Ovine Pancreatitis.

Nerves can be severely reshaped in human pancreatic diseases such as chronic pancreatitis (CP) and pancreatic cancer, in which pancreatic nerves can undergo hypertrophy or hyperplasia. This neural plasticity is associated with neuropathic pain. Although there are several animal models of CP, pancreatic neuropathy is not well-characterized. Thus, the translational value of these in-vivo models cannot be entirely ascertained for the study of neural plasticity. We now describe spontaneous alterations characteristic of pancreatic neural plasticity in a lamb. Microscopic lesions of chronic sclerosing pancreatitis were associated with neuronal hypertrophy and hyperplasia. Although CP and pancreatic tumours are common in many animal species, to the authors' knowledge, spontaneous occurrence of associated pancreatic neural plasticity has not been reported in any non-human species. Sheep might be a suitable animal model for the study of this condition.

Chronic pancreatitis in farmed pigs fed excessive zinc oxide.

Most of the pigs on a farm in Aichi Prefecture, Japan had chronic diarrhea and severe wasting. The pigs had consumed 8,000 ppm zinc oxide (ZnO) as a feed additive. The pancreas of each of 4 autopsied pigs was less than half the normal size. Acinar cells were considerably decreased. Epithelial duct-like cells were increased and tested positive for cytokeratin AE1/AE3, Ki67, PGP9.5, and Sox9. Pancreatic islet cells were decreased and shrunken. The α and δ cells were relatively decreased, and their distribution was abnormal. Islet cells were positive for PGP9.5. The livers and kidneys had high accumulations of zinc (Zn; 788 µg/g and 613 µg/g, respectively). Copper was deficient in the liver, likely as a result of Zn poisoning. Our immunohistologic examination suggested that the high dose of ZnO could influence the function of islet cells in addition to that of acinar cells. Given that colistin sulfate has been banned as a feed additive in order to reduce antimicrobial use in Japan, the use of ZnO in the livestock industry is expected to increase. Zn supplementation of pig feed must be monitored to prevent Zn poisoning and contamination of soil and water.

Chronic Inflammatory Disease in the Pancreas, Kidney and Salivary Glands of English Cocker Spaniels and Dogs of Other Breeds Shows Similar Histological Features to Human IgG4-related Disease.

Chronic pancreatitis (CP) is a common disease in the English cocker spaniel (ECS) and is characterized histologically by duct destruction, interlobular fibrosis and dense periductular and perivenous lymphocytic aggregates. These features are also found in human autoimmune pancreatitis type 1, part of a glucocorticoid-responsive, multiorgan syndrome, newly recognized as IgG4-related disease (IgG4-RD). Human IgG4-RD affects one or several organs, often showing a predominance of IgG4+ plasma cells histologically, with an IgG4+:total IgG+ plasma cell ratio of >40%. This study investigated whether ECSs with CP and/or inflammatory disease in several organs show an increase in IgG4+ plasma cells within affected tissues. Histological sections of pancreas, liver, kidney, salivary gland and conjunctiva were obtained from ECSs with idiopathic chronic inflammatory disease affecting those tissues. Tissue samples from age-matched dogs of other breeds with similar diseases were also sampled. Control diseased tissue samples, from dogs without a suspected immune-mediated disease, were included. A subset of ECSs and dogs of other breeds presented with disease in more than one organ. Immunohistochemistry was performed with primary reagents detecting total IgG and three of the four canine IgG subclasses (IgG2, IgG3 and IgG4). Normal sections of pancreas and liver showed an absence of labelled plasma cells of any subclass. Normal kidney and salivary gland sections showed the presence of a few labelled plasma cells (<10 plasma cells/high-power field). Fourteen tissue sections from 12 ECSs and seven sections from six dogs of other breeds showed elevated numbers of IgG4+ plasma cells and IgG4+:IgG+ ratios >40%. Individual dogs (ECSs and other breeds) showed marked increases in IgG4+ cells. There were no significant differences in the number of IgG4+ plasma cells between ECSs and dogs of other breeds for affected pancreas, liver, salivary glands and conjunctiva. Kidney sections had more IgG4+ cells, for both ECSs and dogs of other breeds, than did sections from other organs. Dogs of other breeds had significantly more IgG4+ plasma cells in affected kidneys than ECSs. In conclusion, several ECSs and dogs of other breeds fulfilled the histological criteria for the diagnosis of IgG4-RD, supporting the existence of a multiorgan immune-mediated disease in ECSs and some dogs of other breeds.

Saikosaponin d ameliorates pancreatic fibrosis by inhibiting autophagy of pancreatic stellate cells via PI3K/Akt/mTOR pathway.

Chronic pancreatitis is characterized by pancreatic fibrosis, associated with excessive activation of pancreatic stellate cells (PSCs) and increased expression of transforming growth factor-ß1 (TGF-ß1). Recently, our studies have shown that autophagy inhibitor could inhibit PSCs activation and reduce collagen secretion. Saikosaponin d (SSd), the major active component of bupleurum falcatum (a medicinal plant), has anti-fibrosis effects in liver. However, it is unclear whether SSd has a role in pancreatic fibrosis. This study aimed to investigate the effect of SSd on the autophagy and activation of PSCs in vivo and in vitro. In vivo, a rat chronic pancreatitis model was induced by intravenous injection of dibutyltin dichloride. SSd was administered at a dose of 2.0 mg/kg body weight per day by gavage. After 4 weeks, the pancreas was collected for histological and molecular analysis. In vitro, PSCs were isolated and cultured for treatment with different dosages of SSd. The results showed that SSd inhibited PSCs autophagy and activation while also reducing extracellular matrix (ECM) formation and pancreatic damage. SSd inhibited autophagy through activating the PI3K/Akt/mTOR pathway. SSd also promoted degradation of ECM with an increasing ratio of MMPs/TIMPs and suppressed the TGF-ß1/Smads pathway. From these results, we concluded that SSd prevents pancreatic fibrosis by reducing autophagy of PSCs through PI3K/Akt/mTOR pathway, which has crosstalk with the TGF-ß1/Smads pathway.

Prevalence of pancreatic, hepatic and renal microscopic lesions in post-mortem samples from Cavalier King Charles spaniels.

OBJECTIVES: The objective of this study was to describe the prevalence of microscopic pancreatic, hepatic and renal lesions in post-mortem samples from Cavalier King Charles spaniels. METHODS: The prevalence of microscopic lesions was determined by routine histopathology and compared to ante-mortem clinical signs. RESULTS: There was evidence of chronic pancreatitis in 51·9% of the cases, and age correlated with severity. Renal lesions were diagnosed in 52·2% of cases, most of which were inflammatory. Ante-mortem diagnosis of pancreatic and renal disease was 25 and 16·7%, respectively. Primary hepatic lesions were diagnosed in 11·1% of cases; secondary hepatic lesions were diagnosed in 64·8%. CLINICAL SIGNIFICANCE: Pancreatic and renal lesions are common in Cavalier King Charles spaniels, but they have similar rates of hepatic disease as the general population. The increasing prevalence of pancreatic lesions with age suggests that it might be a progressive condition.

Chronic Pancreatitis with Acinar-Ductal Metaplasia and Ductal Dysplasia in a Horse.

A 16-year-old Friesian gelding with relapsing colic was humanely destroyed during diagnostic laparotomy due to suspected abdominal neoplasia. On post-mortem examination, the pancreas appeared as a firm mass (20 × 8 × 8 cm). The cut surface had a lobular structure with multiple cavities. Histological examination revealed severe chronic fibrosing pancreatitis with acinar-ductal metaplasia and duct dysplasia, which was considered to be the cause of the recurrent colic. Formation of tubular complexes within a background of acinar-ductal metaplasia is similar to the regressive lesions detected in the human pancreas in the context of inflammation, duct obstruction, cystic fibrosis and neoplasia. Pancreatic acinar-ductal metaplasia and ductal dysplasia are considered to be preneoplastic conditions in man and in the mouse.

Pancreatitis and diabetes in cats.

Pancreatitis is an important potential cause and complicating factor in cases of diabetes mellitus. Pancreatitis can lead to development of diabetes mellitus, which may be transient (diabetic remission) or permanent through destruction and loss of ß cells. Pancreatitis can also be a complicating factor in management of diabetic cats by exacerbating or inducing peripheral insulin resistance, particularly at times of intensified pancreatitic inflammation. Pancreatitis is commonly associated with other inflammatory conditions-especially inflammatory bowel disease and cholangiohepatitis-and its presence makes management of diabetes mellitus more challenging.

Chronic pancreatitis in dogs: a retrospective study of clinical, clinicopathological, and histopathological findings in 61 cases.

The objective of this study was to characterize the clinical, clinicopathological, and histopathological findings of dogs with chronic pancreatitis. The necropsy database at Texas A&M University was searched for reports of dogs with histological evidence of chronic pancreatitis defined as irreversible histologic changes of the pancreas (i.e. fibrosis or atrophy). A reference necropsy population of 100 randomly selected dogs was used for signalment and concurrent disease comparisons. Cases were categorized as clinical or incidental chronic pancreatitis based on the presence of vomiting, decreased appetite, or both vs. neither of these signs. All archived pancreas samples were scored histologically using a published scoring system. Sixty-one dogs with chronic pancreatitis were included. The most frequent clinical signs were lethargy, decreased appetite, vomiting, and diarrhea. Compared to the reference necropsy population, chronic pancreatitis cases were more likely to be older, neutered, of the non-sporting/toy breed group, and to have concurrent endocrine, hepatobiliary, or neurological disease. Clinical cases had significantly higher histological scores for pancreatic necrosis and peripancreatic fat necrosis, and were significantly more likely to have hepatobiliary or endocrine disease as well as increased liver enzyme activities, or elevated cholesterol and bilirubin concentrations. In conclusion, clinical disease resulting from chronic pancreatitis might be related to the presence of pancreatic necrosis and pancreatic fat necrosis. The signalment, presentation, and concurrent diseases of dogs with chronic pancreatitis are similar to those previously reported for dogs with acute pancreatitis.

Chronic pancreatitis in dogs.

Chronic pancreatitis used to be considered uncommon in dogs, but recent pathological and clinical studies have confirmed that it is in fact a common and clinically significant disease. Clinical signs can vary from low-grade recurrent gastrointestinal signs to acute exacerbations that are indistinguishable from classical acute pancreatitis. Chronic pancreatitis is a significant cause of chronic pain in dogs, which must not be underestimated. It also results in progressive impairment of endocrine and exocrine function and the eventual development of diabetes mellitus or exocrine pancreatic insufficiency or both in some affected dogs at end stage. The etiology is unknown in most cases. Chronic pancreatitis shows an increased prevalence in certain breeds, and recent work in English Cocker Spaniels suggests it is part of a polysystemic immune-mediated disease in this breed. The histological and clinical appearance is different in different breeds, suggesting that etiologies may also be different. Diagnosis is challenging because the sensitivities of the available noninvasive tests are relatively low. However, with an increased index of suspicion, clinicians will recognize more cases that will allow them to institute supportive treatment to improve the quality of life of the patient.

Pancreatitis in cats.

Pancreatitis was considered a rare disease in the cat until a couple of decades ago when several retrospective studies of severe acute pancreatitis were published. It was apparent that few of the diagnostic tests of value in the dog were helpful in cats. With increasing clinical suspicion, availability of abdominal ultrasonography, and introduction of pancreas-specific blood tests of increasing utility, it is now accepted that acute pancreatitis is probably almost as common in cats as it is in dogs, although the etiology(s) remain more obscure. Pancreatitis in cats often co-exists with inflammatory bowel disease, less commonly with cholangitis, and sometimes with both. Additionally, pancreatitis may trigger hepatic lipidosis, while other diseases, such as diabetes mellitus, may be complicated by pancreatitis. Therapy is similar to that used in dogs, with added emphasis on early nutritional support to prevent hepatic lipidosis. Less is known about chronic pancreatitis than the acute form, but chronic pancreatitis is more common in cats than it is in dogs and may respond positively to treatment with corticosteroids.

Characterization of chronic pancreatitis in English Cocker Spaniels.

BACKGROUND: Chronic pancreatitis (CP) is common in dogs. The cause is unknown. In humans, different causes of pancreatitis have histologically distinct appearances. The histopathologic lesions in English Cocker Spaniels (ECS) with CP were noted to be histologically different than those of other breeds with CP. HYPOTHESIS: CP in ECS is distinct from CP in other breeds and is characterized by a duct destruction similar to what is observed in autoimmune CP of humans. ANIMALS: Eight ECS and 9 other breeds with histologically confirmed CP recruited over an 8-year period and 50 postmortem control dogs with CP. METHODS: Clinical, clinicopathological, and ultrasonographic findings were recorded. Histological sections were compared with a normal dog and 59 dogs of other breeds with CP. Immunohistochemistry using anti-CD3, anti-CD79a, and anti-cytokeratin antibodies was used to evaluate distribution and type of lymphocytic inflammation and appearance of pancreatic ducts. RESULTS: Four male and 4 female ECS presented at a mean age of 7.2 years. Clinical signs were similar in ECS and other breeds. The pancreas was enlarged and hypoechoic in 4 ECS and 2 controls. Histopathology was characterized by interlobular and periductular fibrosis and inflammation in ECS compared with intralobular disease in most other breeds. Immunohistochemistry identified prominent anti-CD3(+) lymphocytic infiltrates around venules and ducts and a marked absence of interlobular ducts in ECS compared with mixed T-cell infiltration and ductular hyperplasia in most other breeds with CP. CONCLUSIONS AND CLINICAL IMPORTANCE: CP in ECS is distinct from CP in other breeds and is notably duct destructive.

Pancreatite crônica intersticial e caquexia causada por Eurytrema coelomaticum em vaca Nelore / Chronic interstitial pancreatitis and chronic wasting disease caused by Eurytrema coelomaticum in Nelore cow

A euritrematose bovina, causada por Eurytrema coelomaticum, tem sido relatada no Brasil. A doença pode afetar animais domésticos, incluindo ruminantes. Estes parasitos geralmente vivem nos ductos pancreáticos e ocasionalmente nos ductos biliares. Este estudo relata um quadro de caquexia em um bovino parasitado por E. coelomaticum proveniente de um rebanho de gado de corte localizado no Estado de Minas Gerais. O animal acometido apresentou perda progressiva de peso, glicosúria e cetonúria. Na necropsia o pâncreas apresentava-se diminuído de tamanho, brancacento, intensa e difusamente firme (fibrose). Vários ductos apresentavam-se dilatados e repletos de Eurytrema. Microscopicamente foi observada destruição extensa do parênquima pancreático e fibrose, ovos e parasitas intralesionais, hiperplasia ductal e inflamação multifocal crônica. Este relato descreve a perda progressiva de peso e pancreatite crônica associada a E. coelomaticum em bovino de corte no Estado de Minas Gerais.

Type 1 diabetes mellitus and hyperadrenocorticism in a ferret.

Diabetes mellitus (DM) was diagnosed in a 6-year-old neutered male ferret with polyuria/polydipsia, symmetrical alopecia, and weight loss. Laboratory tests revealed severe hyperglycemia, glucosuria, and increased steroid hormone profile. Abdominal ultrasound revealed a bilateral enlargement of the adrenal glands. Significant clinical improvement was achieved with insulin- and leuprolide acetate-based therapy. After 2 months of therapy, the ferret showed a severe ketoacidosis, and the owner decided to euthanize the animal. Histological findings revealed carcinoma of the left adrenal cortex and cortical hyperplasia of the right adrenal gland. Moderate, chronic, and active pancreatitis with a marked decrease in the number of beta-cells was also present. This is the first reported case of type 1 DM associated with hyperadrenocorticism and chronic pancreatitis in a ferret.

Observational study of 14 cases of chronic pancreatitis in dogs.

This study reports the clinical, clinicopathological and ultrasonographic findings from dogs with chronic pancreatitis (CP). Fourteen dogs with clinical signs consistent with CP and histological confirmation of the disease were evaluated. Abdominal ultrasound and clinical pathology results were recorded. Sensitivities of pancreatic enzymes for diagnosis of CP were calculated with two different cut-off values. The mean age of affected dogs was 9.1 years. Spaniels were the most common breed with CP, representing seven of the 14 dogs in this study. CP was histologically severe in nine cases. Most dogs showed chronic low-grade gastrointestinal signs and abdominal pain. Five dogs had exocrine pancreatic insufficiency and five dogs had diabetes mellitus. The sensitivity of elevated trypsin-like immunoreactivity for CP was 17 per cent. The sensitivities of canine pancreatic lipase immunoreactivity, lipase and amylase for CP were 44 to 67 per cent or 14 to 28 per cent depending on the cut-off value used. Cholesterol was elevated in 58 per cent of samples. Liver enzymes were often elevated. The pancreas appeared abnormal on 56 per cent of ultrasound examinations. Ten dogs had died by the end of the study period; only one case was due to CP.

Chronic pancreatitis with secondary diabetes mellitus treated by use of insulin in an adult California sea lion.

CASE DESCRIPTION: A 21-year-old neutered male captive California sea lion developed chronic polyuria; polydipsia; polyphagia; accelerated development of existing cataracts; and frequent episodes of gastrointestinal upset including anorexia, signs of abdominal discomfort, diarrhea, and vomiting. CLINICAL FINDINGS: Chronic hypercholesterolemia, hypertriglyceridemia, hyperglycemia, and glucosuria were identified. During episodes of gastrointestinal abnormalities, transient hyperbilirubinemia and increased serum J-glutamyltransferase activities developed. Clinical findings strongly suggested chronic pancreatitis with secondary diabetes mellitus and intermittent cholestasis. Multiple diagnostic tests, including abdominal ultrasonography, serial hematologic and serum biochemical analyses, fecal examinations, urinalyses and bacteriologic culture of urine, measurement of serum fructosamine and insulin concentrations, and evaluation of thyroid and adrenal function, did not reveal any specific parasitic, endocrine, hepatic, or neoplastic etiologies. TREATMENT AND OUTCOME: For 1.5 years, the sea lion received once-daily administration of glargine insulin, gastrointestinal protectants, and a strict high-protein, low-fat diet. Daily monitoring of glucose regulation was achieved by training the sea lion to submit to blood and urine sampling. Glucose regulation ranged from fair to good, and clinical signs of diabetes mellitus lessened. Episodes of gastrointestinal upset still occurred, although the frequency and severity decreased. Ultimately, a severe episode developed, associated with diabetic ketoacidosis and sepsis, and the sea lion died. Severe fibrosing pancreatitis with exocrine and endocrine atrophy and abscesses arising from ectatic pancreatic ducts were found. Peripancreatic fibrosis caused stricture of the common bile duct, resulting in gallbladder distension without cholecystitis. CLINICAL RELEVANCE: Diabetes mellitus can occur secondary to chronic pancreatitis in California sea lions and insulin therapy should be considered.

Chronic pancreatitis in dogs and cats.

Pancreatitis is the most common disorder of the exocrine pancreas in dogs and cats. Clinical diagnosis of chronic pancreatitis is challenging because the disease is usually mild or subclinical and because its clinical signs are often the same as those of complicating or concurrent diseases. Obtaining a detailed history, performing a thorough physical examination, and conducting tests that are sensitive and specific for pancreatitis are crucial in diagnosing chronic pancreatitis. Initial management of an acute episode of chronic pancreatitis largely involves supportive and dietary measures, while long-term management of chronic pancreatitis is based on dietary modification. Management of complications and concurrent diseases is crucial in animals with chronic pancreatitis.

Endocrine pancreatic insufficiency secondary to chronic herpesvirus pancreatitis in a cockatiel (Nymphicus hollandicus).

A cockatiel (Nymphicus hollandicus) examined because of weight loss, polydipsia, and polyuria was diagnosed with diabetes mellitus based on the presence of glucosuria and marked hyperglycemia. Medical attempts to manage the diabetes mellitus were unsuccessful, and the bird was euthanatized. Histopathologic examination of the pancreas revealed a chronic active pancreatitis with herpesviral inclusions in many of the pancreatic acinar and duct cells. Psittacid herpesvirus-1 (PsHV-1) DNA was amplified from the lesion by polymerase chain reaction. Sequencing of the amplicon showed it to be the genotype 1 variant, which is most commonly associated with Pacheco's disease, an acute rapidly fatal systemic infection. The findings in this case suggest that the PsHV-1 genotype may also cause a localized disease of the pancreas. Infection with this virus should be considered as a differential diagnosis in birds with pancreatitis with or without diabetes mellitus.