Histopathological and immunohistochemical investigations of the hepatic compartment associated with parasitism and serum biochemical changes in canine visceral leishmaniasis

Abstract

The immunopathological evaluation of the hepatic compartment associated with parasitism and biochemical findings are essential for understanding the genesis of hepatomegaly in canine visceral leishmaniasis (CVL). Three clinical groups of dogs naturally infected with Leishmania chagasi [i.e., asymptomatic (AD, n=12), oligosymptomatic (OD, n=12) and symptomatic (SD, n=17)] were assessed and compared with a group of non-infected dogs (NID, n=11). Intense reaction of the Kupffer cells, capsule and portal inflammation, and the presence of intralobular granulomas, were observed in the different clinical groups. Dogs in the SD group presented a higher frequency of parasitism compared with the AD group. Inflammatory alterations were more intense in the SD group and were associated with parasitism. Our results indicated an association between histological liver changes and the progression of biochemical alterations according to progression of clinical forms of CVL, and the direct relationship between clinical symptoms and frequency of hepatic parasitism.

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

“…43,120 Hepatomegaly, which is far more often a pathologic than clinical finding, is the result of inflammatory infiltrate, hypertrophy/hyperplasia of resident cells, and possibly passive congestion. 43,62,120 Fibrogenesis in the liver of CanL cases has been positively correlated to parasitic load, clinical status of the infected dogs, and degenerative changes observed in the hepatic parenchyma. 62,88 CanL-induced hepatitis, although informative from a clinicopathologic point of view, is actually a subclinical condition (sensu stricto), as the cases that are admitted with liver failure are very few, at least according to our experience.…”

Relationship between clinical and pathological signs and severity of canine leishmaniasis

“…In addition, high parasite loads in the components of mononuclear phagocyte system (MPS), e.g., in bone marrow and liver, triggering the occurrence of clinical pathology related to hepatic and hematopoietic functions (KEENAN et al, 1984b;AMUSATEGUI et al, 2003). Considering that parasite density in tissues increase according to the severity of clinical manifestations (GIUNCHETTI et al, 2006;REIS et al, 2006b), symptomatic dogs present significantly decreased levels of albumin and increased levels of globulin fraction, leading to an inversion of A/G ratio when compared to asymptomatic dogs, suggesting a relationship between the presence of exacerbated clinical forms of CVL, serum protein levels and humoral immune response alterations (GIUNCHETTI et al, 2006(GIUNCHETTI et al, , 2008REIS et al, 2006b). Biochemical findings in CVL include alterations in the hepatic enzymes aspartate aminotransferase, alanine aminotransferase and alkaline phosphatase (SLAPPENDEL, 1988;ABRANCHES et al, 1991).…”

Análise histomorfométrica da matriz extracelular do linfonodo poplíteo de cães naturalmente infectados por Leishmania (L.) chagasi

“…Em estudo realizado em linfonodos provenientes de diversas regiões do corpo de cães infectados por L. chagasi (Lima et al 2004), foi observada linfadenopatia generalizada com maior proeminência nos linfonodos cervicais e poplíteos, histologicamente explicada pelo aumento do tamanho e do número dos folículos linfóides. Cães com LCV apresentaram maior reação medular dos linfonodos quando comparados com cães não-infectados (Giunchetti et al 2007). Neste estudo evidenciou-se também a presença de colágeno circundando os folículos linfóides (Fig.2B), edema subcapsular (Fig.2C) e presença de infiltrado inflamatório na cápsula do linfonodo (Fig.2D).…”

“…Apesar da avaliação histopatológica qualitativa de folículos linfóides dos cães portadores de leishmaniose visceral ter mostrado maior reatividade dos centros germinativos quando comparados com os cães sadios, as análises morfométricas comprovaram numericamente que não há diferença significativa em nível de 5% (p>0,05) (Quadro 5). De modo semelhante aos achados deste estudo, foi observado que em cães sintomáticos infectados por L. chagasi, ocorre atrofia da região cortical sugerindo que este fato aconteça como resultado da diminuição do número de células nos centros germinativos, ocasionada por um mecanismo imunorregulador, como por exemplo, a apoptose (Giunchetti et al 2007). Em outro estudo (Lima 2004) é descrito que, histologicamente, os linfonodos de cães oligossintomáticos, especialmente o cervical superficial e o poplíteo, mostram hiperplasia nodular.…”