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.