BackgroundLeishmania spp. are zoonotic protozoans that infect humans and other mammals such as dogs. The most significant causative species in dogs is L. infantum. In dogs, leishmaniosis is a potentially progressive, chronic disease with varying clinical outcomes. Autochthonous cases of canine leishmaniosis have not previously been reported in the Nordic countries.ResultsIn this report we describe the first diagnosed autochthonous cases of canine leishmaniosis in Finland, in which transmission via a suitable arthropod vector was absent. Two Finnish boxers that had never been in endemic areas of Leishmania spp., had never received blood transfusions, nor were infested by ectoparasites were diagnosed with leishmaniosis. Another dog was found with elevated Leishmania antibodies. A fourth boxer dog that had been in Spain was considered to be the source of these infections. Transmission occurred through biting wounds and semen, however, transplacental infection in one of the dogs could not be ruled out.Two of the infected dogs developed a serious disease and were euthanized and sent for necropsy. The first one suffered from membranoproliferative glomerulonephritis and the second one had a chronic systemic disease. Leishmania sp. was detected from tissues by PCR and/or IHC in both dogs. The third infected dog was serologically positive for Leishmania sp. but remained free of clinical signs.ConclusionsThis case report shows that imported Leishmania-infected dogs may pose a risk for domestic dogs, even without suitable local arthropod vectors.
This study was conducted to determine whether the seasonal delay in puberty in autumn is driven by individual differences in night-time melatonin secretion in domestic gilts at the attainment of puberty. A group of spring-born gilts (n = 30) were expected to reach puberty in autumn by the age of 7 months. Eighteen of these gilts were selected in pairs on the basis of matched days of birth. By the expected time, half of the animals showed oestrous symptoms (group CYCLING, n = 9) with the rest remaining silent (group SILENT, n = 9). Afterwards, all gilts were fitted with indwelling jugular catheters for frequent blood sampling. Blood samples were collected from all animals three times during the day followed by three times in the night at 2-h intervals for 48 h. The samples were analysed by a commercial radioimmunoassay (RIA). The results show a consistent 25-fold rise (on average) in night-time melatonin concentration in every animal sampled with group averages ranging from 0.28 +/- 0.04 to 0.37 +/- 0.06 pg/ml at day and from 10.20 +/- 2.16 to 10.67 +/- 0.05 pg/ml at night. Night-time group mean values between CYCLING and SILENT gilts did not differ significantly (10.26 +/- 0.67 and 10.38 +/- 0.94 for the CYCLING; 10.67 +/- 0.05 and 10.20 +/- 2.16 for the SILENT). When 10 pg/ml was used as a threshold value, six individuals did not reach it during the night (low responders). Two of these gilts were CYCLING and four were SILENT. In conclusion, the results presented imply no involvement of the level of night-time melatonin concentration in the seasonal delay of puberty in gilts.
Mycobacteriosis caused by non-tuberculous mycobacteria (NTM) is a rising concern in human medicine both in immunocompromised and immunocompetent patients. In cats, mycobacteriosis caused by NTM is considered mostly to be a focal or dermal infection, with disseminated disease mostly caused by Mycobacterium avium. We describe three cases of disseminated mycobacteriosis in cats, caused by Mycobacterium malmoense, Mycobacterium branderi/shimoidei and M. avium, with no identified underlying immunosuppression. In all cases, extracellular mycobacteria were seen in the pulmonary epithelium, intestinal lumen and glomerular tufts, which could affect the shedding of the organism. The present study highlights the importance of mycobacteriosis as a differential even in immunocompetent animals. Considering the close relationship of owners and pets and the potential presence of free mycobacteria in secretions, cats should be considered as a possible environmental reservoir for mycobacteria.
Background: Shaking puppy syndrome is commonly attributed to abnormal myelination of the central nervous system.Hypothesis/Objectives: To report the long-term clinical course and the imaging characteristics of hypomyelinating leukodystrophy in German Shepherd dogs.Animals and Methods: Three related litters with 11 affected dogs.Results: The 11 affected dogs experienced coarse, side-to-side tremors of the head and trunk, which interfered with normal goal-oriented movements and disappeared at rest. Signs were noticed shortly after birth. Nine dogs were euthanized, 3 dogs underwent pathological examination, and 2 littermates were raised by their breeder. Tremors improved gradually until 6 to 7 months of age. Adult dogs walked with severe residual pelvic limb ataxia. One dog developed epilepsy with tonic-clonic seizures at 15 months of age. Conventional magnetic resonance imaging (MRI) disclosed homogenous hyperintense signal of the entire subcortical white matter in 3 affected 7-week-old dogs and a hypointense signal in a presumably unaffected littermate. Subcortical white matter appeared isointense to gray matter at 15 and 27 weeks of age on repeated MRI. Abnormal white matter signal with failure to display normal gray-white matter contrast persisted into adulthood. Cerebellar arbor vitae was not visible at any time point. Clinical signs, MRI findings, and pathological examinations were indicative of a hypomyelinating leukodystrophy. All parents of the affected litters shared a common ancestor and relatedness of the puppies suggested an autosomal recessive mode of inheritance. Conclusion:We describe a novel hypomyelinating leukodystrophy in German Shepherd dogs with a suspected inherited origin.
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