Emphysematous pyometra and emphysematous hepatitis caused by Klebsiella pneumoniae infection in a diabetic dog.

A 14-year-old intact female diabetic dog presented with seizures and hyperglycemic hyperosmolar syndrome. Radiographs revealed gas-filled tubular structures in the right and left caudal abdomen, raising concerns of emphysematous pyometra or small intestinal ileus. Ultrasonography played a pivotal role in confirming emphysematous pyometra, a technique previously documented only once in veterinary practice. This report also presents the first documented case of emphysematous pyometra in a diabetic dog attributed to Klebsiella pneumoniae and complicated by emphysematous hepatitis.

Potential therapeutic effect of thymoquinone and/or bee pollen on fluvastatin-induced hepatitis in rats.

Hepatitis is one of earlier, but serious, signs of liver damage. High doses of statins for a long time can induce hepatitis. This study aimed to evaluate and compare the therapeutic potential of thymoquinone (TQ) and bee pollen (BP) on fluvastatin (F)-induced hepatitis in rats. Rats were randomly divided into: group 1 (G1, control), G2 (F, hepatitis), G3 (F + TQ), G4 (F + BP), and G5 (F + TQ + BP). Single treatment with TQ or BP relieved fluvastatin-induced hepatitis, with best effect for the combined therapy. TQ and/or BP treatment significantly (1) reduced serum levels of alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, gamma glutamyl transpeptidase, and total bilirubin, (2) decreased malondialdehyde levels and increased level of reduced glutathione, and activities of glutathione peroxidase and catalase in the liver, (3) improved liver histology with mild deposition of type I collagen, (4) increased mRNA levels of transforming growth factor beta 1, nuclear factor Kappa B, and cyclooxygenase 1 and 2, and (5) decreased tumor necrosis factor alpha and upregulated interleukin 10 protein in the liver. These data clearly highlight the ability of TQ and BP combined therapy to cause better ameliorative effects on fluvastatin-induced hepatitis than individual treatment by each alone.

Traumatic reticuloperitonitis combined with embolic pneumonia and hepatitis as unusual symptoms of foreign body syndrome in a Holstein bull.

Traumatic reticuloperitonitis combined with embolic pneumonia and hepatitis is unusual signs of foreign body syndrome in cattle. A 4-year-old Holstein bull presented decreased appetite, dry cough, progressive weight loss, sternal recumbence and reluctance to stand and move. Laboratory tests revealed leucocytosis (18.4 × 103 /µl) accompanied by neutrophilia (10.48 × 103 /µl), and monocytosis (1.28 × 103 /µl), hyperglobulinaemia (6.3 g/dl), hypoalbuminaemia (1.5 g/dl), hyperfibrinogenaemia (10 g/L) and severe increase in gamma-glutamyl transferase activity (1,216 U/L). Reticular ultrasonographical examination showed a large amount of hyperechoic and hypoechoic content between the reticular serosa and the hepatic visceral surface. The main gross findings included fibrin deposition and adhesions between the reticulum, liver and diaphragm surfaces; a 4.0 mm in diameter transmural reticular perforation; a 12.0-cm diameter and scarce small randomly abscesses in the liver's parenchyma. The lungs presented multifocal areas of suppurative embolic foci (pulmonary abscesses), interstitial emphysema and multifocal fibrin deposition on the pleural surface. Ancillary diagnostic tests, such as ultrasonography and laboratory test, associated with clinical evaluation, may increase the accuracy of the correct diagnosis and avoid wasting time and money on untreatable cases.

Canine copper-associated hepatitis: A retrospective study of 17 clinical cases.

Background: Copper-associated hepatitis (CAH) is a well-documented chronic hepatic disease in dogs. In some breeds, the disease results from an inherited defect in copper metabolism. In others, it is unclear whether its acummulation is a primary or secondary condition. Reports of copper accumulation in dog breeds that are not genetically predisposed are increasing. Aim: To describe the epidemiology, clinical and laboratory findings, liver biopsy techniques, and treatment response in dogs with CAH. Methods: A retrospective study was performed, drawing upon medical records from CAH dogs at a Veterinary Referral Hospital in Paris, France. The diagnosis of CAH had been confirmed in these patients by positive rhodanine staining of hepatic tissue obtained through biopsy. Medical records were mined for the following data: age at presentation, sex, breed, chief presenting complaints, abdominal ultrasound (US) findings, and rhodanine staining pattern. Results: A total of 17 dogs were included in the study. Median age at presentation was 8-year old (4-11). No sex predisposition was found. Terriers (4/17) and German Shepherd Dogs (GSD, 3/17) were overrepresented. American Staffordshire Terriers and Beauceron had not previously appeared in case reports on CAH; two of each breed were identified in this study. Clinical signs of affected dogs were non-specific. An incidental identification of increased liver-enzymes was observed in 5/17 dogs. A heterogeneous, mottled liver was frequently described (5/17) on abdominal US. Liver biopsies were performed by US-guided percutaneous approach in 10/17 dogs, laparoscopy and laparotomy in 6/17 and 1/17, respectively. The rhodanine staining pattern was centrilobular (zone 3) in 8/17 dogs and periportal (zone 1) in 3/17 dogs. The pattern was considered multifocal in 6/17 dogs. Conclusion: Increased liver enzymes may be the only clinical finding in dogs with copper-associated hepatitis, reflecting the silent progression of this disease. Centrilobular pattern of rhodanine staining was observed in the majority of cases suggesting the primary condition of the disease. Results of this study are consistent with the current literature, which reports that terriers and GSD are predisposed to CAH. This is the first description of CAH in Beauceron and American Staffordshire Terrier dogs.

Pathobiology and diagnosis of clostridial hepatitis in animals.

Clostridia can cause hepatic damage in domestic livestock, and wild and laboratory animals. Clostridium novyi type B causes infectious necrotic hepatitis (INH) in sheep and less frequently in other species. Spores of C. novyi type B can be present in soil; after ingestion, they reach the liver via portal circulation where they persist in phagocytic cells. Following liver damage, frequently caused by migrating parasites, local anaerobic conditions allow germination of the clostridial spores and production of toxins. C. novyi type B alpha toxin causes necrotizing hepatitis and extensive edema, congestion, and hemorrhage in multiple organs. Clostridium haemolyticum causes bacillary hemoglobinuria (BH) in cattle, sheep, and rarely, horses. Beta toxin is the main virulence factor of C. haemolyticum, causing hepatic necrosis and hemolysis. Clostridium piliforme, the causal agent of Tyzzer disease (TD), is the only gram-negative and obligate intracellular pathogenic clostridia. TD occurs in multiple species, but it is more frequent in foals, lagomorphs, and laboratory animals. The mode of transmission is fecal-oral, with ingestion of spores from a fecal-contaminated environment. In affected animals, C. piliforme proliferates in the intestinal mucosa, resulting in necrosis, and then disseminates to the liver and other organs. Virulence factors for this microorganism have not been identified, to date. Given the peracute or acute nature of clostridial hepatitis in animals, treatment is rarely effective. However, INH and BH can be prevented, and should be controlled by vaccination and control of liver flukes. To date, no vaccine is available to prevent TD.

Inclusion Body Herpesvirus Hepatitis in Captive Falcons in the Middle East: A Review of Clinical and Pathologic Findings.

Inclusion body hepatitis in falcons is caused by a herpesvirus designated Falconid HV-1. This herpesvirus and other herpesviruses affecting birds of prey have not been assigned to a genus and include inclusion body herpesvirus hepatitis in eagles (Accipitrid HV-1) and inclusion body herpesvirus hepatitis in owls (Strigid HV-1). Herpesvirus infections have been diagnosed in both captive and free-living raptors across Europe, North America, and Asia in different species of the family Falconidae. Herpesviruses affecting owls and falcons have been found to be antigenically similar to pigeon herpesvirus (Columbid HV-1) and distinct from other avian herpesviruses. When the herpesvirus isolates from owls, falcons, and pigeons were compared by sequencing a fragment of the herpes viral DNA polymerase gene from those birds naturally infected with the virus, the sequences from these 3 sources were found to be nearly identical. The authors of this study concluded that the Falconid HV-1, Strigid HV-1, and Columbid HV-1 were the same virus. Furthermore, the authors also proposed that the virus therefore be referred to as Columbid HV-1 (CoHV-1), because pigeons may be responsible for the transmission of the virus to birds of prey. Pigeons are often carriers of the virus without showing any clinical signs. It has long been suspected that raptors may contract the infection by the ingestion of infected pigeons. Some studies have suggested that falcons may not contract the infection through the oral route by ingesting carrier pigeons, but through the ocular or nasal route. Inclusion body herpesvirus hepatitis is a frequently diagnosed disease in the captive falcon population used for falconry, racing, and breeding in the Middle East, and it seems to be associated with the extensive use of pigeons for training and as a food item. This paper reviews the clinical and pathological findings in falcons affected by inclusion body herpesvirus hepatitis in the Middle East.

Molecular detection and characterization of fowl adenovirus associated with inclusion body hepatitis from broiler chickens in Egypt.

A case-control study was performed to assess prescence of inclusion body hepatitis (IBH) caused by fowl adenoviruses (FAdVs) at Kafr EL-Shiekh Governorate, Egypt, during spring, 2017. The case group consisted of 100 liver and spleen samples collected from 10 broiler chickens flocks (10 samples from each flock) suspected to be infected with IBH depending on clinical manefestations and necropsy examination. Controls were randamly selected from chickens without clinical sings or evidence of the disease on postmortem examination. Molecular screening of the disease disease in collected samples based on the DNA polymerase gene of FAdVs was carried out. Furthermore, the DNA polymerase gene sequence was determined and analyzed with published reference sequences on GeneBank. Respectively, enzyme-linked immunosorbent assay (ELISA) and reverse transcription-polymerase chain reaction (RT-PCR) were used to confirm existence of co-infection with chicken infectious anemia virus (CIAV) and/or infectious bursal disease virus (IBDV in flocks involved in the study. Using PCR, FAdV genome was detected in seven flocks in the case group and one in the control group. FAdV identified in this study revealed close genetic relationship with FAdVs-D previously identified in UK and Canada, suggesting potential virus transmission from these countries. All tested serum samples from diseased chickens were positive for CIAV infection via ELISA while none of the collected bursa of Fabricius samples tested IBDV positive by RT-PCR. Therefore, results obtained from the current study highlighted the importance of implementation of control measures against FAdV and CIAV in Egyptian poultry flocks. This study opens the door for future work toward specific identification of FAdV serotypes circulating in Egyptian poultry farms and molecular characterization of the virus based on hexon gene or full genome sequencing for better understanding of genetic diversity among FAdVs in Egypt at higher reolution.

Pneumatosis of the intestines, colon and liver in a young cat.

To describe a case of naturally occurring pneumatosis intestinalis, pneumatosis coli and emphysematous hepatitis in a cat. A 9-month-old, indoors-only, female spayed, domestic medium hair cat presented for vomiting, open-mouth breathing and acute collapse. The initial physical examination identified moderate to severe hypothermia [35°C (95°F)], obtunded mentation, weak femoral pulses, tachycardia (heart rate 240 beats per min), pale pink mucous membranes and significant splenomegaly on abdominal palpation. Immediate diagnostics performed [packed cell volume and total solids (PCV, TS), venous blood gas and electrolytes] revealed severe anaemia (PCV 12%), hypoproteinaemia (TS = 2.2 g/dl), and severe metabolic acidosis (pH 6.956). Additional diagnostics performed included Feline Leukaemia Virus and Feline Immunodeficiency Virus testing (FeLV/FIV), complete blood count (CBC) with pathology review, serum biochemistry profile, prothrombin time (PT) and partial thromboplastin time (PTT), urinalysis, and abdominal radiographs. Abdominal radiographs were consistent with gas within hepatic and splenic veins and parenchyma, small intestinal walls and colonic wall. Due to the guarded prognosis, euthanasia was elected. Necropsy was performed and the most significant gross and histopathological findings included intra-luminal and intra-mural intestinal haemorrhage and vascular congestion with mild neutrophilic hepatitis, and marked hepatic periportal emphysema. Clostridium perfrigens and Escherichia coli were cultured from the bowel wall; no bacterial growth from the liver or spleen was identified. This case report describes idiopathic emphysematous hepatitis, with concurrent emphysema of the spleen and intestinal wall and intestinal haemorrhage. To the authors' knowledge, this type of pathology in a feline patient has not been previously described.

Infectious necrotic hepatitis caused by Clostridium novyi type B in a horse: case report and review of the literature.

A 14-y-old bay Quarter Horse gelding was presented with progressive neurologic signs, elevated rectal temperature, and icterus for 3 d prior to death. Postmortem examination revealed icterus, large amounts of serosanguineous fluid in the abdominal cavity, widespread petechiae and ecchymoses in several organs, and a large, pale, and well-demarcated focus of necrosis in the liver. Histologically, there was coagulative necrosis surrounded by a rim of inflammatory cells and large numbers of gram-positive rods, which were identified as Clostridium novyi by immunohistochemistry. Liver samples tested by PCR were positive for C. novyi type B flagellin and alpha toxin genes, but negative for Clostridium haemolyticum and other clostridia. Based on postmortem findings and ancillary tests, a definitive diagnosis of infectious necrotic hepatitis (INH) was made. Mostly a disease of ruminants, also known as black disease, INH has rarely been reported in horses, and a definitive etiologic diagnosis has not been achieved previously; the etiology of all cases reported to date was identified as C. novyi but the type was not determined. Animals are predisposed to clostridial hepatitis when hepatic anaerobiosis is established. Such conditions allow germination and proliferation of bacterial spores, resulting in production and release of toxins. INH, caused by C. novyi type B, and bacillary hemoglobinuria, caused by C. haemolyticum, are mechanistically and pathologically almost indistinguishable. Because these 2 microorganisms are closely related, differentiation requires molecular tools.

Cholangitis and Cholangiohepatitis in Dogs: A Descriptive Study of 54 Cases Based on Histopathologic Diagnosis (2004-2014).

BACKGROUND: Cholangitis in dogs appears to be more common than previously thought, but understanding of the disease remains incomplete. OBJECTIVE: To describe a population of dogs with cholangitis or cholangiohepatitis. ANIMALS: Fifty-four client-owned dogs with cholangitis or cholangiohepatitis. METHODS: Medical records of dogs with cholangitis or cholangiohepatitis confirmed by histopathology between January 2004 and December 2014 were identified using a computer-based search and retrospectively reviewed. RESULTS: Clinical signs included vomiting (72.2%), lethargy (70.4%), and inappetence (64.8%). Most dogs (49/50) had increased liver enzyme activities, hyperbilirubinemia (32/50), and hypercholesterolemia (24/43). Ultrasonographic abnormalities of the hepatobiliary system were seen in 84% of cases. On histopathology, 53 of 54 affected dogs had neutrophilic cholangitis (NC) or cholangiohepatitis, whereas 1 dog had lymphocytic cholangitis. Most cases (42/54) were chronic. Evidence of concurrent biliary disease (46.2%) and biliary tract obstruction (42.6%) was common. Seventeen of 36 biliary and 11 of 25 liver cultures were positive for bacterial growth; Escherichia coli and Enterococcus spp. were most common. Median patient survival was 671 days (95% confidence interval [CI]: 114-1,426). On Cox regression, dogs that did not have a cholecystectomy performed had a 2.1 greater hazard for death (P = 0.037; 95% CI: 1.0-4.3) compared to cholecystectomized dogs. Dogs >13 years old had a 5.0 greater hazard for death (P = 0.001; 95% CI: 1.9-13.2) compared to younger dogs. CONCLUSIONS AND CLINICAL SIGNIFICANCE: Chronic NC or cholangiohepatitis was most common. Cholecystitis and biliary tract obstruction often occurred in conjunction with cholangitis. Cholecystectomized dogs had decreased risk of death; thus, cholecystectomy may improve patient outcome.

Canine Hepatitis Associated with Intrahepatic Bacteria in Three Dogs.

This case report describes the detection of intrahepatic bacteria in formalin-fixed paraffin-embedded histopathological sections from three dogs with neutrophilic, pyogranulomatous, or lymphoplasmacytic hepatitis and cholangiohepatitis. In each of these cases, eubacterial fluorescence in situ hybridization enabled colocalization of intrahepatic bacteria with neutrophilic and granulomatous inflammation in samples that were negative for bacteria when evaluated by routine hematoxylin and eosin histopathology augmented with histochemical stains. Positive responses to antimicrobial therapy were observed in of 2 out of 2 patients that were treated with antimicrobials. These findings suggest that eubacterial fluorescence in situ hybridization analysis of formalin-fixed paraffin-embedded histopathological sections is more sensitive than conventional histochemical stains for the diagnosis of bacteria-associated canine hepatitis.

Antihistone Autoantibodies in Dobermans With Hepatitis.

BACKGROUND: Immune system involvement is suggested as an underlying cause for Doberman hepatitis (DH) based on female predisposition, lymphocyte infiltration, abnormal hepatocyte expression of major histocompatibility complex class II antigens, and homozygosity for dog leukocyte antigen DRB1*00601. OBJECTIVE: To measure serum antinuclear antibodies (ANA) and serum antihistone antibodies (AHA) in Dobermans with hepatitis. To determine whether increased serum ANA or serum AHA could be used to support the diagnosis of Doberman hepatitis (DH). ANIMALS: Privately owned 25 subclinically and 13 clinically affected DH Dobermans and 17 healthy control Dobermans. METHODS: Case-control study. Indirect immunofluorescence (IIF) microscopy and line blot tests were employed for the ANA pilot studies and an enzyme-linked immunosorbent assay (ELISA) assay for detection of IgG AHA. RESULTS: Indirect immunofluorescence revealed ANA-positive cases, and line blot showed AHA reactivity. In ELISA, importantly increased concentrations of AHA were found in 92% (23/25) of dogs in the subclinical stage and 84.6% (11 of 13) of dogs in the clinical stage of DH compared with no control dogs (0/17) (P < 0.0005). The mean AHA absorbance values of the blood samples obtained from the 25 subclinical DH dogs (1.36 ± 0.60, mean ± SD) and the 13 clinically affected dogs (1.46 ± 0.49) were significantly higher than in 17 control dogs (0.51 ± 0.18; P < 0.0001). CONCLUSIONS AND CLINICAL IMPORTANCE: As the presence of AHA indicates autoimmune activity, our results favor an autoimmune background as one cause for DH. Antihistone antibody could represent a novel means for screening Dobermans with increased serum alanine transaminase concentrations and suspicion of DH.

Sensitivity and Specificity of Plasma ALT, ALP, and Bile Acids for Hepatitis in Labrador Retrievers.

BACKGROUND: Biochemical indicators for diagnosing liver disease are plasma alanine aminotransferase activity (ALT), alkaline phosphatase activity (ALP), and bile acid concentration (BA). OBJECTIVES: To determine the sensitivity and specificity of ALT, ALP, and BA for detecting primary hepatitis (PH) in clinically healthy Labrador retrievers and investigate whether ALT and ALP can discriminate between dogs with PH and nonspecific reactive hepatitis (RH). ANIMALS: 191 clinically healthy and 51 clinically ill Labrador retrievers with hepatic histopathology. METHODS: Retrospective study. Medical records were reviewed for ALT, ALP, preprandial BA, liver histopathology, and hepatic copper concentrations. RESULTS: In 64% (122/191) of the clinically healthy Labrador retrievers, hepatic histology revealed inflammatory infiltrates. This frequency might be biased because part of them was included as first-line relatives of dogs with copper-associated hepatitis. Sensitivity of ALT, ALP, and BA in this population for detecting acute hepatitis was 45, 15, and 15%, respectively. For chronic hepatitis, sensitivity was 71, 35, and 13%, respectively. Specificity of ALT, ALP, and BA was >90% for AH, CH, and RH. When increased liver enzymes were present, median ALT was significantly higher in PH cases (312 U/L, range 38-1,369) compared to RH cases (91 U/L, range 39-139) (P < .001). There was no difference in ALP between dogs with a PH and a RH (P = .361). CONCLUSIONS AND CLINICAL IMPORTANCE: Histopathologic abnormalities in the liver were present in the majority of apparent clinically healthy Labrador retrievers. The sensitivity of ALT, ALP, and BA for detecting acute and chronic hepatitis in this population was low. More sensitive biomarkers are needed for early detection of liver disease in apparent clinically healthy dogs.

Acute fatal sarcocystosis hepatitis in an Indo-Pacific bottlenose dolphin (Tursiops aduncus) in Hong Kong.

Unlike most species in the genus Sarcocystis, Sarcocystis canis has a broad intermediate host range. Its life cycle is incompletely known and most reports are from the USA. Here we report fatal hepatitis in a 4year old male Indo-Pacific bottlenose dolphin (Tursiops aduncus) from Hong Kong associated with a S. canis-like infection. Diagnosis was made based on clinical presentation, histopathology, transmission electron microscopy (TEM), and molecular characterization. Microscopically, S. canis-like like infection was confined to the liver. Immature and mature schizonts were found in hepatocytes and the parasite was associated with generalized hepatic necrosis. By TEM, schizonts divided by endopolygeny, and merozoites lacked rhoptries. Molecular characterization of parasites present in liver and brain tissues at the cox1 gene showed a high degree of identity (97-98%) and clustered together with Sarcocystis canis, S. lutrae, S. arctica, S. speeri, S. turdusi, and S. rileyi in a phylogenetic study. This is the first report of S. canis-like infection from Asia.

Canine Copper-Associated Hepatitis.

Copper-associated hepatitis is recognized with increasing frequency in dogs. The disease is characterized by centrolobular hepatic copper accumulation, leading to hepatitis and eventually cirrhosis. The only way to establish the diagnosis is by histologic assessment of copper distribution and copper quantification in a liver biopsy. Treatment with the copper chelator d-penicillamine is the most commonly used treatment. In addition, a low-copper/high-zinc diet can help prevent accumulation or reaccumulation of hepatic copper. Mutations in the copper metabolism genes COMMD1 or ATP7A and ATP7B have been associated with hepatic copper concentrations in Bedlington terriers and Labrador retrievers respectively. In the Labrador retriever, dietary copper intake contributes strongly to the disease phenotype.

Canine Idiopathic Chronic Hepatitis.

The World Small Animal Veterinary Association's Liver Standardization Group produced standardized criteria for the histologic diagnosis of canine chronic hepatitis (CH). They define CH by the presence of hepatocellular apoptosis or necrosis, a variable mononuclear or mixed inflammatory cell infiltrate, regeneration, and fibrosis. There are variations in histologic appearance between breeds. Hepatic copper accumulation is an important cause of canine CH. However, where copper accumulation has been ruled out, dogs are said to have idiopathic CH. This article reviews theories regarding the etiopathogenesis of canine CH other than copper accumulation, and its clinical features, diagnostic findings, and management.

Necrotizing and haemorrhagic hepatitis and enteritis in commercial layer pullets.

This case report describes an episode of recurring severe necrotizing and haemorrhagic hepatitis and enteritis experienced in a flock of commercial layer pullets at 12 weeks of age and again at 18 weeks of age in Indiana. Pullets had been vaccinated at 10 weeks old using a trivalent Salmonella Enteritidis (SE)/Newcastle disease/infectious bronchitis oil-emulsion-inactivated vaccine. The pullets were found dead at 12 weeks with firm but friable, enlarged, haemorrhagic livers, enlarged spleens, and necrohaemorrhagic intestines. Histopathologic findings were consistent with a necrotizing and haemorrhagic enteritis and hepatitis. Livers had multiple intra-sinusoidal thrombi, intestines contained Gram-positive bacterial colonies, and spleens had marked lymphoid depletion. The pullets seemed to improve after antibiotic treatment. Pullets were vaccinated with an inactivated SE vaccine at 14 weeks of age. A second spike of mortality occurred at 18 weeks of age. Although clostridial enteritis and hepatitis were highly suspected in the two cases based on macroscopic and microscopic findings, no significant bacterial or viral agents were isolated from the livers and intestines. In summary, lesions in the liver and intestines are speculated to be due to repetitive vaccination, leading to an anamnestic response by the immune system, and resulting in an immune-mediated response. However, much of the pathogenesis is still unclear, and other causes such as unidentified infectious aetiology, transmissible amyloidosis, and hypersensitivity may need further investigation.