SummaryHamartoma is a developmental disorder of various body parts and organs. It is characterized by a nonneoplastic growth of tissue with an uneven distribution and proportion of individual cells. Lesions progress for several years, but usually do not give clinical symptoms, and do not undergo malignant transformation. They occur alone or coexist with other defects, sometimes forming a characteristic clinical picture of a syndrome of congenital defects. Mutations in genes, such as PTEN, GLI3, SDH B/D, PIK3CA and ACT1, cause a dysfunction of the tumor suppressor gene and result in an increased neoplastic transformation. Hamartoma is a lesion between developmental disorders and benign tumors, which occurs frequently in humans, but is very rare in domestic animals. In a histopathological examination, however, it is diagnosed relatively often. In the veterinary literature, both hamartoma and choristoma are attributed mostly to errors in embryogenesis and are not considered as preneoplastic lesions.

Hypoglycemia is frequently found in dogs suffering from portosystemic shunt (PSS). However, the mechanisms leading to abnormal blood glucose concentration in such dogs have not been studied. Therefore, investigations were undertaken to study the structure of pancreatic islets in 25 patients with congenital PSS (cPSS). Material for morphometry and histopathology was taken during the surgical closing of the abnormal blood vessel. A total of 75 islets (3 randomly chosen from each patient) were analyzed, and their average size was compared to reference values for dogs that were considered as 50-325 μm. The average size of 47 (63%) islets was below 50 μm, whereas the mean dimension of the largest islet did not exceeded 80 μm. The average islet size in all patients was 46 (SD 13.3) μm and in only 2 dogs (8%) all 3 analyzed islets were bigger than the lower reference value. Histopathological examination revealed cytoplasmic vesicles in pancreatic cells, as well as extracellular, homogenous, acidophilic deposits in pancreatic islets. These results indicate that in dogs suffering from cPSS the pancreatic islets are smaller than the reference values and their cells may contain abnormal structures.

Introduction: Farm mink (Neovison vison) can be naturally exposed to T. canis and T. leonina pathogens on the farm. If mink were hosts, it would imply some veterinary public health as well as animal welfare issues. For this reason, the aim of the study was to determine whether mink might be definitive or paratenic hosts of these parasites. Material and Methods: Four groups of mink were infected with both parasite species using larvated eggs or feed containing mouse tissue previously infected with the parasites. Following inoculation, the infections were monitored in vivo by faecal examination for 14 weeks p.i., and then western blotting and ELISA were performed. Results: Coprology did not reveal any canine roundworm eggs, neither were nematodes found in mink intestines during post mortem examination. The specific IgG antibodies recognising excretory/secretory (ES) antigens of both parasite species were identified in mink sera. Single T. leonina tissue larvae were found in digested organs. Conclusions: Our results confirm that farm mink may contribute both T. canis and T. leonina infections. It was proved that farm mink were not their definitive hosts, and therefore mink faeces need not be considered a source of canine roundworm eggs in any soil it fertilises. Nonetheless, as farm mink may be a paratenic host for both parasite species, this may have some impact on the health and welfare of infected animals.

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Subcutaneous dirofilariosis in dogs, caused by Dirofilaria repens, is an underdiagnosed disease, now recognized for its zoonotic potential, and growing distribution and prevalence across Europe and Asia. Our understanding of the pathogenicity in human and canine host remains unclear, but case reports suggest that microfilariae (Mf) as well as adult D. repens may directly cause internal organs damage or may be a factor complicating the course of other ailments. The purpose of the study was to report high Mf in dogs and to discuss potential relevance with co-morbidity. Our data from a modified Knott's test performed on 62 infected dogs indicate that the median Mf count in D. repens infections is 675 Mf/ml and we consider microfilaremia above 10,000 Mf/ml as high intensity. This collection of case reports discusses 4 cases of high intensity D. repens microfilaremia in companion dogs; one presenting pathology from a very high intensity of adult D. repens with post-treatment complications, and 3 dogs in which high microfilaremia was detected incidentally during the management of other primary illnesses. To our knowledge this report describes the highest D. repens microfilaremia ever detected in a dog, at 178,000 Mf/ml. The issue of high microfilaremic infections in dogs is poorly studied and there is growing need to identify the presentation and understand the mechanisms of associated pathogenesis in the host-parasite relationship.

This study evaluated the effect of Artemisia absinthium and Malva sylvestris on antioxidant response and histopathological changes in the abomasa of the Haemonchus contortus infected lambs. Twenty-four lambs were divided into four groups: unsupplemented lambs (UNS), lambs supplemented with A. absinthium (ART), lambs supplemented with M. sylvestris (MAL), and lambs supplemented with both plants (ARTMAL). Lambs were infected orally with approximately 5000 third-stage (L3) larvae of H. contortus. The experiment was conducted for 75 d (days), all animals were then slaughtered; and the abomasal tissues were examined for antioxidant parameters and histopathology. The concentration of malondialdehyde in the abomasal mucosa was lower in ARTMAL (p < 0.05), and the total antioxidant capacity was higher in MAL (p < 0.05), than in UNS. Increased mucus production was observed in the ARTMAL. The number of mast cells in UNS and ART was significantly higher than the number in MAL (p < 0.01 and p < 0.05). Plasma cell numbers were higher in ARTMAL than the number in MAL (p < 0.05). Abomasal tissue regenerated more frequently in ARTMAL. These results represent the first report of the impact of A. absinthium and M. sylvestris on antioxidant parameters and local immune responses of abomasal mucosa of lambs infected with a GIN parasite.

Hepatic stellate cells play a crucial role in the development of liver fibrosis. In a damaged liver, stellate cells undergo activation, which is manifested as a change of their phenotype: differentiation of stellate cells to myofibroblast-type cells, expression of alpha-Smooth Muscle Actin, their proliferation and a reduction in the size of cytoplasmic lipid droplets. The aim of this study was to determine the number and morphology of stellate cells in the canine liver affected by congenital portosystemic shunt (PSS) and portal vein hypoplasia – hepatic microvascular dysplasia (PVH-HMD). The material for investigation were archived paraffin blocks with liver samples collected supravitally from six dogs with PSS, six dogs with PVH-HMD and six healthy dogs. On the HE-stained sections, the number of stellate cells per 100 hepatocytes was counted (Sztark method) and the diameter of veins in the hepatic triads was measured (light microscope Olympus BX 43, SC30 camera, CellSens Entry 2011 Olympus). In addition, the diameter of lipid droplets in stellate cells was measured (computed image analysis system LUCIA 4.21). The results were analysed statistically (the Kruskal-Wallis test followed by Dunn’s post-hoc procedure; significance level (α) at 0.05; Statistica 12 StatSoft Inc.). The degree of liver fibrosis was determined (Masson’s method of slide stain; Scheuer scale). The liver samples from the dogs with PSS and PVH-HMD were stained immunohistochemically with Monoclonal Mouse Anti-Human Smooth Muscle Actin (α-SMA), clone 1A4, antibodies (DAKO). Portosystemic shunt and primary portal vein hypoplasia in the dog results in a reduction in the diameter of portal vein branches and in insufficient portal blood flow through the liver. In the material investigated, this was particularly evident in the animals affected by PSS: such dogs had a significantly smaller diameter of the veins than did the healthy dogs (p<0.001) or the dogs with PVH-HMD (p=0.023). Fibrosis and the expression of α-SMA were stronger in the dogs with PSS than in those with PVH-HMD. Moreover, the dogs with PSS had a significantly higher average number of stellate cells than the healthy animals (p=0.007) did. However, the examination of the material revealed an enlargement of cytoplasmic lipid droplets: the dogs with PSS had a significantly larger diameter of lipid vacuoles in the cytoplasm of stellate cells than did the healthy animals (p<0.001) or the dogs with PVH-HMD (p=0.043); the dogs with PVH-HMD had lipid droplets with a significantly larger diameter than the healthy animals (p<0.001) did. Hypoperfusion of the liver and the accompanying regressive lesions in hepatocytes result mainly in an increased number of stellate cells and stronger expression of α-SMA, while cytoplasmic lipid droplets in the stellate cells are not reduced in size. The present study indicates the need for detailed analyses of clinical cases and warrants further comprehensive studies of comparative hepatopathology because it demonstrates differences between humans and dogs in the morphological indicators of hepatic stellate cell activation in chronic liver damage.

Introduction: The clinical symptoms of portosystemic shunts (PSSs) and hepatic microvascular dysplasia (HMD) – portal vein hypoplasia (PVH) in dogs are similar. PSSs are abnormal vascular connections between the portal vein system and systemic veins. HMD is a very rare developmental vascular anomaly, recognisable during histopathological examination. The study aim was to assess the prevalence of HMD–PVH and hepatocellular and vascular pathologies in the liver. Material and Methods: Liver biopsies from 140 dogs (of different breeds and both sexes) arousing clinical suspicion of PSS were examined histopathologically. Results: An initial PSS diagnosis was confirmed in 125 dogs (89.29%). HMD–PVH was found in 12.32% of dogs, as an isolated disease in 9.29%, especially in Yorkshire terriers, and with extrahepatic PSS in 6.67%. Histopathological analysis of muscles around sublobular veins showed that HMD cases presented hypertrophy or hypertrophy with fibrosis. In 2.17% of all dogs with liver vascular developmental disorders calcification was visible around vessels (without correlation by degenerative changes in those vessels), suggesting prior onset of deep metabolic disorders. Clinical suspicion of PSS was also formed upon quite different pathological processes in young dogs. Conclusion: Histopathological findings diagnosed the type of vascular anomalies (PSS or HMD–PVH) or other pathological changes conclusively, therefore detailed hepatic histopathology is an indispensable component of the clinical diagnostic process.