In dogs with symptomatic or asymptomatic leishmaniosis, Leishmania infantum appears to induce a mixed Th1/Th2 immune response that in the sick dog may eventually result in tissue damage via different pathomechanisms, notably granulomatous inflammation (eg, nodular dermatitis, osteomyelitis), immune complex deposition (eg, glomerulonephritis), and/or autoantibody production (eg, polymyositis). This is a compensatory but detrimental mechanism generated mainly because of the insufficient killing capacity of macrophages against the parasite in the susceptible dog. Clinical disease is typically exemplified as exfoliative and/or ulcerative dermatitis, with or without nasodigital hyperkeratosis and onychogryphosis, glomerulonephritis, atrophic myositis of masticatory muscles, anterior uveitis, keratoconjunctivitis sicca, epistaxis, and/or polyarthritis, appearing alone or in various combinations. The pathogenesis of these clinical conditions has recently been highlighted, to a greater or lesser extent. The usually subclinical conditions expressed as chronic colitis, chronic hepatitis, vasculitis, myocarditis, osteomyelitis, orchiepididymitis, and meningoencephalomyelitis, though uncommon, are of pathologic importance from a differential point of view. The leading cause of death among canine leishmaniosis patients is chronic proteinuric nephritis that may progress to end-stage kidney disease, nephrotic syndrome, and/or systemic hypertension. However, even the asymptomatic proteinuria, when profuse, may be a serious problem because it predisposes to arterial thromboembolism and eventually contributes to the deterioration of the body condition.

Background: Canine leishmaniasis (CanL) is a common cause of epistaxis in dogs residing in endemic areas. The pathogenesis of CanL-associated epistaxis has not been fully explored because of the limited number of cases reported so far.Hypothesis: Epistaxis in CanL could be attributed to more than 1 pathomechanism such as hemostatic dysfunction, biochemical abnormalities, chronic rhinitis, and coinfections occurring in various combinations.Animals: Fifty-one dogs with natural CanL. Methods: The allocation of 51 dogs in this cross-sectional study was based on the presence (n 5 24) or absence (n 5 27) of epistaxis. The potential associations among epistaxis and concurrent infections (Ehrlichia canis, Bartonella spp., and Aspergillus spp.), biochemical and hemostatic abnormalities, and nasal histopathology were investigated.Results: Hypergammaglobulinemia (P 5 .044), increased serum viscosity (P 5 .038), decreased platelet aggregation response to collagen (P 5 .042), and nasal mucosa ulceration (P 5 .039) were more common in the dogs with epistaxis than in those without epistaxis. The other significant differences between the 2 groups involved total serum protein (P 5 .029) and g-globulin (P 5 .013) concentrations, which were higher, and the percentage platelet aggregation to collagen, which was lower (P 5 .012) in the epistaxis dogs.Clinical Importance: CanL-associated epistaxis appears to be the result of multiple and variable pathogenetic factors such as thrombocytopathy, hyperglobulinemia-induced serum hyperviscosity, and nasal mucosa ulceration.

In canine leishmaniosis, the parasitic density of the skin may be important for the infection of sandflies, and increased accumulation of inflammatory cells infected with Leishmania is believed to occur in dermal areas subjected to mechanical trauma. Parasite density and inflammatory responses in the upper and lower dermis of three body sites: flank (control site), dorsal muzzle (sandfly feeding site), and footpads (mechanical stress sites) were thus investigated in 15 dogs with symptomatic leishmaniosis. Parasite density did not differ between the control and tested sites or between the upper and lower dermis, apart from the footpads where it was higher in the upper dermis, and there was no correlation with severity of the macroscopic lesions or inflammatory infiltrate, except for the lower footpad dermis. No selective accumulation of the parasite in the muzzle that would favour its transmission to sandflies occurred, and the mechanical stress imposed on the footpads was not associated with increased parasitic density, or with inflammatory infiltrate.

Twenty domestic shorthaired (DSH) and 20 Siamese (S) kittens were allocated into 4 breed-specific groups, of 10 kittens each, that were fed exclusively cooked sardines (F groups) or commercial feline canned food based on oily fish (C groups) for a 4-month period. Clinical signs were scored every 15 d along with body weight recording and blood sampling for the measurement of alpha-tocopherol and selenium (Se) concentrations and glutathione peroxidase (GSH-Px) activity. Subcutaneous adipose tissue samples were obtained per month to determine its fatty acid composition. Steatitis, reproduced in all 20 F-group kittens, was accompanied by systemic signs in 5 DSH and 6 S animals. The severity of the disease reached its zenith at the second week in the DSH-F-group kittens and the fourth and sixth week in the S-F-group kittens. alpha-Tocopherol plasma level was significantly lower in F groups compared to their corresponding controls, whereas the opposite was true for Se and red blood cell GSH-Px activity. In conclusion, the results of this study have shown that although the morbidity rate is not different between the two breeds, the delay of Siamese cats to develop symptomatic steatitis is presumably attributed to an inherent resistance as a result of the long-standing evolution of more efficient antioxidant mechanisms. Also, the changes in fatty acid composition of the adipose tissue lipids are associated with the progression of the age, breed, and diet and probably with the inflammatory changes of the adipose tissue.

Long-term management of MVD in dogs could benefit from the serial measurement of cTnI.