Visceral Leishmaniasis in the German Shepherd Dog. II. Pathology

Abstract

Three German shepherd dogs were inoculated with Leishmania chagasi and three with Leishmania donovani and the infection was followed for 82 days. All infected dogs developed splenomegaly and lymphadenomegaly. In lymph nodes there was a reduction in lymphocyte population in paracortical areas, extensive proliferation of macrophages in paracortical areas and medullary cords, follicular hyperplasia, and increased numbers of plasma cells. The spleen had decreased numbers of lymphocytes in periarteriolar lymphoid sheaths, proliferation of macrophages in these regions, follicular hyperplasia, and enlargement of the red pulp with clusters of macrophages and plasma cells. The morphology of the tonsil was similar to the lymph nodes. Clusters of macrophages, often containing Leishmania spp, were present in liver, bone marrow, lung, and the intestines. The morphologic changes in lymph nodes and spleen were suggestive of a suppressed cell-mediated immunity and an active humoral immunity. The German shepherd dog may be a useful laboratory model for the study of immunopathologic changes in visceral leishmaniasis.

Chronic interstitial pneumonitis in dogs naturally infected with Leishmania (Leishmania) chagasi: a histopathological and morphometric study

“…In dogs, pulmonary lesions are very similar to those observed in humans, and were previously characterized by some authors as interstitial pneumonitis mainly characterized by thickening of alveolar walls associated with the presence of a chronic cellular exudate mainly consisting of macrophages 1,23 . Later on, similar lesions were described in dogs experimentally infected with Leishmania (Leishmania) chagasi 13 .…”

Inhibition of receptor tyrosine kinases restores immunocompetence and improves immune-dependent chemotherapy against experimental leishmaniasis in mice

“…For example, the observed decrease in splenic IL-10 may, in addition to promoting increased APC function (22,53), directly facilitate parasite killing within macrophages exposed to IFN-γ and TNF production (54). Similarly, alterations in IFN-γ induced by Sm preconditioning may also have effects on the local uptake and accumulation of Sb v within macrophages (45), contributing to the reduction in ED 50 we observed. Defining the relative contribution of these different pathways will require the future application of complex mouse models in which selective function can be ablated in a cell-specific and temporal manner.…”

“…Nevertheless, we believe that from the available evidence, changes similar to those reported here in mice may occur in humans. First, in spite of clear anatomical differences in the microarchitecture of rodent and human spleen (33), H&E studies of human spleens taken from postmortem VL patients show white pulp atrophy, with loss of germinal centers, depletion of lymphocytes (presumptive T cells), follicular disruption, and extensive macrophage egress into the tissue (29,49), all histopathologic changes that were also observed in experimental VL (17,20) and in canine VL (50). Second, studies in canine VL have provided clear electron microscopical evidence for microvascular changes associated with progressive disease (34), data confirmed here by a variety of other approaches in experimental murine VL.…”

Relationship between clinical and pathological signs and severity of canine leishmaniasis

“…The analysis revealed dysproteinemia, azotemia and anemia as the main laboratory findings in dogs naturally infected with different clinical forms of visceral leishmaniasis. According to the literature, anemia is considered a common finding in CVL (KEENAN et al, 1984a;FERRER 1992). It is likely that more than one factor is involved in the etiology of anemia, such as hemorrhage, hemolysis, chronic renal failure, bone marrow hypoplasia or aplasia, and decreased lipid fluidity of the erythrocyte membrane (SLAPPENDEL; GREENE, 1990;BURILLO et al, 1994;KOUTINAS et al, 1999;DE LUNA et al, 2000).…”