Canine visceral leishmaniasis with amyloidosis: An immunopathological case study

Corbeil, Lynette B.; Wright-George, J.; Shively, James N.; Duncan, J.R.; LaMotte, G.B.; Schultz, Ronald D.

doi:10.1016/0090-1229(76)90107-0

Cited by 12 publications

(5 citation statements)

References 13 publications

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“…In both canine and hamster experimental infections, the renal abnor malities described are the results of short-term experi ments, in a selected canine breed or in golden hamsters, with selected species of visceral Leishmania, such as the Khartum strain and L.chagasior L.donovani 1, S, respec tively [17,18], The results of these studies revealed monomorphic renal lesions which were quite different from those found in human and canine natural leishmaniasis. In fact, in both experimental conditions, after the devel opment of mesangial proliferative GN, cellular prolifera tion was replaced in a very short time by the deposition of amyloid material, a finding which seems to be sporadic in the natural series [8,9,19]. In our study, amyloid deposits were a sporadic observation outlining the importance of specific factors related with the host immune response associated with the synthesis and deposition of amyloid.…”

Section: Discussionmentioning

confidence: 62%

“…In our study, amyloid deposits were a sporadic observation outlining the importance of specific factors related with the host immune response associated with the synthesis and deposition of amyloid. It has been postulated that this factor may be identified in plasma cell dysfunction [8], The difference between the patterns of glomerular abnormalities found in dogs and hamsters with experimentally induced leishmaniasis and the spontaneous type is considerable and gives a warning as to how experimental models may not be representative of the natural evolution of tissue lesions.…”

Section: Discussionmentioning

confidence: 99%

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Renal Involvement in Canine Leishmaniasis

Poli¹,

Abramo²,

Mancianti³

et al. 1991

Nephron

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In a prospective survey in the Isle of Elba, 413 dogs affected by naturally acquired Leishmania infantum infection were identified out of a controlled population of 1,500 resident mongrel dogs. In all the 34 randomly selected dogs of different breed, age, and duration of disease, the presence of glomerular lesions which defined mainly two categories of glomerulonephritis (GN) was observed. The first group was characterized by mesangial-cell proliferation either with focal features (11 dogs), or with a diffuse pattern (10 dogs). The second group (12 dogs) showed the typical findings of segmental membrano-proliferative GN; amyloid deposits were seen in the glomerular tuft and interstitium in 1 dog. Immunohistochemical investigation revealed granular deposits of IgG, IgM, and C₃ both in mesangial areas as well as on glomerular capillary walls. Granular immune deposits on the tubular basement membrane were also found in 31 out of 34 dogs examined. With ultrastructural investigation, subendothelial and mesangial electron-dense deposits were revealed. Age, sex, serum creatinine, BUN, duration of disease, anti- Leishmania antibody titers, and immune complexes did not discriminate between the types of observed GN, while proteinuria did. The study shows that the renal involvement is the natural sequela in dogs infected with L. infantum, and that the kidney lesions are characterized by immunologically mediated glomerular and tubular damage.

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Section: Discussionmentioning

confidence: 62%

Section: Discussionmentioning

confidence: 99%

Renal Involvement in Canine Leishmaniasis

Poli¹,

Abramo²,

Mancianti³

et al. 1991

Nephron

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“…This reaction originates as a response to the presence of leishmanias inside the macrophages, which multiply in their cytoplasm in an uncontrolled way since these cells are unable to destroy them. Progressively, and due to the antigenic stimulation of these parasites, a hyperactivation of humoral immunity (CORBEIL et al, 1976) takes place and, as a result, there is infiltration of lymphocytes and plasma cells along with the parasited macrophages.…”

Section: Discussionmentioning

confidence: 99%

Erosive Colitis in Experimental Canine Leishmaniasis

Gonzalez

Fermín

García

et al. 1990

Journal of Veterinary Medicine, Series B

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Summary Six 4 month‐old beagles were inoculated with Leishmania infantum, three of them intraperitoneally (Group A) and the other three intravenously (Group B). The animals from Group A were killed at 109, 433 and 592 days after inoculation and animals from Group B 109, 171 and 334 days after inoculation. At 350 days (Group A) and 275 days (Group B) after inoculation, dogs started to develop a chronic large bowel diarrhoea. At necropsy a diffuse colonic and rectal wall thickening of gradually increasing severity was observed. Histological examination of the colon showed a diffuse inflammatory infiltration of the mucosa and submucosa by macrophages with amastigotes, lymphocytes, plasma cells and some neutrophils and eosinophils. The surface epithelium developed increasingly extensive degeneration, which caused the development of erosions on the mucosal surface. The crypts of Lieberkühn decreased in number and showed degeneration of the crypt epithelium.

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“…Eventually most of the cel lular organelles are replaced by amyloid. This process of amyloid fibril development was also shown by Corbeil et al [ 1976] in a case of secondary amyloidosis in a dog.…”

Section: Discussionmentioning

confidence: 77%