Granulocytic ehrlichiosis in two dogs in Switzerland.

This case report describes two dogs with granulocytic ehrlichiosis. Dog 1 was a male Labrador retriever with clinical signs of lymphosarcoma. Dog 2 was a female Airedale terrier, whose clinical signs included apathy, pyrexia, diarrhea, and abdominal pain. Examination of blood smears revealed Ehrlichia organisms in the neutrophils of both dogs. There was thrombocytopenia in both dogs, and dog 2 also had leukopenia. In both dogs, bands of identical length were amplified from DNA of leukocytes via nested PCR. The bands had identical nucleotide sequences, which differed from the gene sequences of Ehrlichia equi and E. phagocytophila in three and two positions, respectively. Interestingly, the nucleotide sequence of the 16S rRNA was 100% homologous to that of a human granulocytic ehrlichia.

Feline mucopolysaccharidosis VII due to beta-glucuronidase deficiency.

A male cat 12-14 weeks old had walking difficulties and an enlarged abdomen. Facial dysmorphism, plump paws, corneal clouding, granulation of neutrophils, vacuolated lymphocytes, and a positive urine test for sulfated glycosaminoglycans suggested mucopolysaccharidosis. Cultured fibroblasts incorporated 35SO4 into mucopolysaccharides more actively than did fibroblasts of a feline control, and degradation was far inferior. Activity of beta-glucuronidase was absent in leukocytes and markedly reduced in fibroblasts, thus establishing the diagnosis of mucopolysaccharidosis VII, a disorder previously described in humans, dogs, and mice. Light microscopic examination revealed foam cells in virtually all organs examined, and electron microscopic examination showed pancytic storage of floccular material characteristic of mucopolysaccharides. Stored sphingolipids in the form of zebra bodies were seen in ganglion cells of the central nervous system and in smooth muscle cells of blood vessels. This case represents another animal model of mucopolysaccharidosis VII with the full disease characteristics known in human patients.

[Key-Gaskell syndrome in a cat in Switzerland]. / Key-Gaskell-Syndrom bei einer Katze in der Schweiz.

As far as the authors know this is the first case of Key-Gaskell-syndrome being described in Switzerland. The clinical signs of megaoesophagus, anorexia, constipation, dryness of all mucous membranes, reduced tear production, protrusion of the membrana nictitans, mydriasis, regurgitation and bradycardia are pathognomonic and can't be mistaken by any other disease. The subject of the Key-Gaskell-syndrome is a dysfunction of the autonomic nervous system. Histopathological changes are exclusively related to the autonomic nervous system and to neurons of some nuclei in the cranial nerves. Less severe changes can be found in the neurons of the spinal cord or in the dorsal root ganglia. The etiology remains still unclear. There is a relationship to the grass sickness syndrome in horses and to dysautonomia of man and dog.