Halzoun, an allergic pharyngitis syndrome in Lebanon: the trematode Dicrocoelium dendriticum as an additional cause.

Halzoun syndrome typically manifests in the form of an allergic pharyngitis following the consumption of raw or undercooked ovine liver. First described in Lebanon in 1905, it was initially attributed to Fasciola hepatica, while later publications have attributed it to other pathogens. There has been no definitive documentation of the pathogen causing the Lebanese Halzoun syndrome. The aim of our study was to identify the parasite responsible for the pathogenesis of the Lebanese Halzoun syndrome. 32 patients with typical clinical symptoms of Halzoun syndrome were recruited in the emergency room at our hospital from 2005 to 2007. One parasite was isolated from a patient's expectorations, and two others were isolated from pieces of a raw sheep liver retrieved from the patients' dishes. A piece of infected goat liver intended for consumption was also collected from a local butcher. All parasites were examined microscopically for identification. All patients presented with immune allergic-like symptoms of the eyes, ears, nose, or throat. All collected parasites were identified as Dicrocoelium dendriticum. Our study has identified D. dendriticum, rather than Linguatula serrata or F. hepatica, as the prime suspect in the pathogenesis of the Lebanese Halzoun syndrome.

Dicrocoelium dendriticum: a true infection?

Dicrocoelium dendriticum is a liver parasite of ruminants. Humans are occasionally infected by ingestion of intermediate hosts. We report a rare case of dicrocoeliasis in a 55-year-old woman who presented with eosinophilia and elevated bilirubin. Therapy with albendazole eradicated the parasite and normalized blood parameters.

Seudoparasitismo por Dicrocoelium dendriticum / Pseudoparasitism of Dicrocoelium dendriticum

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Immunohistochemical study of the local immune response in lambs experimentally infected with Dicrocoelium dendriticum (Digenea).

Phenotypic expression of inflammatory cells in liver and hepatic lymph nodes (HLN) has been examined in lambs experimentally infected with Dicrocoelium dendriticum using immunohistochemical techniques. Thirty-two lambs, 12 infected with 1,000 D. dendriticum metacercariae, 12 with 3,000, and 8 controls were used. Half the lambs in each group were slaughtered on days 60 and 180 post-infection (p.i.), respectively. Primary antibodies (Abs) against T cell epitopes (CD3+, CD4+, CD8+ and WC1+ gammadelta), B cell epitopes (CD79alphacy+, CD45R+), immunoglobulin (IgG)-bearing plasma cells, macrophages (CD14+, VPM32+) and major histocompatibility complex (MHC) class IIbeta antigen were used. T lymphocytes (CD3+, CD4+ and CD8+) and B lymphocytes (CD79alphacy+ and CD45R+) with diffuse pattern or forming lymphoid aggregates and follicles surrounded the septal bile ducts (SBD) and inter-lobular bile ducts, whereas the WC1 gammadelta T cells were scattered. Numerous IgG+ plasma cells were observed around SBD. CD14 and VPM32+ macrophages intermingled with lymphocytes were immunostained by the anti-MHC class IIbeta. This Ab also reacted with lymphoid cells. Likewise, increased positive immunostaining for all Abs used was observed in the HLN of infected lambs. There was no qualitative difference regarding the phenotype expression of inflammatory cells between the lambs infected with D. dendriticum. The humoral and cell-mediated local immune responses observed were similar in the two groups of lambs infected with different doses.

Hepatic marker enzymes, biochemical parameters and pathological effects in lambs experimentally infected with Dicrocoelium dendriticum (Digenea).

Hepatic enzymes and biochemical parameter values were analysed in the sera of 32 lambs: 12 infected with 1,000 Dicrocoelium dendriticum metacercariae, 12 with 3,000 and eight controls. Blood samples were collected at intervals of 30 days from day 0 post-infection (p.i.). Half the lambs in each group were slaughtered on days 60 and 180 p.i, respectively. A histopathological and ultrastructural study was carried out on the liver, gall bladder and hepatic lymph nodes of all animals. A minute increase was detected in the bilirubin (7%) and albumin (3%) values in the infected lambs (with 30-2,063 worms) in comparison with those of the controls. The hepatic enzyme values did increase, above all aspartate aminotransferase (19%) and alanine aminotransferase (22%), mainly in the lambs tested with 3,000 metacercariae (38% and 48%, respectively). The increase was significant 60 days p.i. The severity of the lesions was closely associated with the parasite burden.

Morphologic and biochemical changes caused by experimentally induced dicroceliosis in hamsters (Mesocricetus auratus).

BACKGROUND AND PURPOSE: The aim of the study reported here was to investigate the pathomorphologic changes caused by experimentally induced dicroceliosis and their correlation with hepatobiliary function. METHODS: Studies were carried out at days 80 and 120 after oral inoculation of hamsters with 40 metacercariae of Dicrocoelium dendriticum. RESULTS: The parasite-induced pathologic changes were assessed by presence of fluke eggs in feces, increased plasma alanine transaminase and aspartate transaminase activities and morphologic alterations. Dicroceliosis was characterized by bile ductular proliferation and enlargement of the bile duct surface area caused by hyperplastic cholangitis in septal bile ducts. The liver from infected animals contained portal tracts infiltrated with small to moderate numbers of lymphocytes, macrophages, and eosinophils. Simultaneously, there was an increase in portal tract collagen that extended to the interlobular septa and caused pressure atrophy of the hepatic parenchyma. The concentration of thiobarbituric acid-reactive substances and the ratio of oxidized to reduced glutathione, measured as markers of oxidative stress, were significantly increased. CONCLUSIONS: The presence of oxidative alterations could be related to the morphologic evidence of chronic inflammatory response as well as to liver cellular injury indicated by cellular swelling, and increased presence of peroxisomes and lysosomes.