Pathologic Mechanisms Underlying the Clinical Findings in Canine Leishmaniosis due to Leishmaniainfantum/chagasi

Abstract

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.

Relationship betweenLeishmaniaIFAT Titer and Clinicopathological Manifestations (Clinical Score) in Dogs

“…Our results are in accordance with Poli et al [21] who, in a study of glomerular lesions in dog with CanL, found no correlation between renal involvement and anti- Leishmania titer and creatinine but found correlation between glomerular lesions and the amount of proteinuria. Glomerulopathy that characterized CanL causes proteinuria due to deposition of circulating antigen/antibody complexes; this fact may explain the correlation between UP/UC and IgG value found in our study [18]. Renal damage with less than 75 percent of nonfunctional nephrons may not cause increase of serum creatinine concentration [22]; therefore, elevation of this parameter during CanL may show up later than the presence of protein in the urine.…”

Insights on adaptive and innate immunity in canine leishmaniosis

“…In sick dogs, the depletion of T lymphocytes in lymphoid organs becomes falsely compensated B-cell proliferation and activity (Koutinas and Koutinas, 2014). This activity, along with the activity of plasma cells, histiocytes and macrophages, potentially explains the generalized lymphadenomegaly, splenomegaly and hyperglobulinemia, which have become clinical hallmarks of this disease (Baneth et al 2008; Koutinas and Koutinas, 2014).…”

Histological and parasitological distinctive findings in clinically-lesioned and normal-looking skin of dogs with different clinical stages of leishmaniosis

“…However, other less typical manifestations such as papular dermatitis, muco-cutaneous nodular dermatitis or sterile pustular dermatitis are also diagnosed [5, 6]. This clinical variation is due to a wide variety of pathological mechanisms occurring secondarily to the inflammation, immune complex deposition and/or autoantibody production [7] and to the genetically determined or acquired inability of the immune system to control parasite multiplication and tissue invasion [8]. …”