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Poster
Contents

Abstract

Introduction

Materials
& Methods

Results

Discussion
& Conclusion

References



Discussion
Board

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Title: Amebiano Hepatic Abscess.

Analysis morphologic and ultrastructural. Report of a case.


Contact Person: Alberto G Pizarro (rediegal@homonet.com.mx)


Discussion & Conclusion

The amebiasis is caused by the trophozoites breakthrough amebics to the raices porches of the submucosa colonic, of where are transported to the liver. The hepatic infection tends be produced in patient with infectation amebiana chronicle or subclínica, and rarely, during a fit of colitis amebiana acute. About half of the patients do not present history that suggest colitis amebiana preceding. (7,8,9)

Amebic abscess of the liver:

Virulence factors that may enable E. histolytica to invade include a galactose-specific adhesin, secreted proteases, extracellular matrix receptors, and a cell surface lipophosphoglycan.(6,7,8,9)

Adherence to and contact-dependent killing of host cells requires the galactose-inhibitable lectin, a heterodimeric glycoprotein composed of heavy and light subunits.(6,7)

Amebic cytolysis of target cells requires Gal/GalNAc-lectin-mediated adherence, parasite phospholipase A activity, and maintenance of an acid pH in amebic intracellular vesicles. Cytolytic activity is stimulated by phorbol esters (activators of protein kinase C) and results from an E. histolytica-mediated increase in free Ca++ within the target cell.(8)

When they reach the liver, the amebas provoke enzimatic focal necrosis of hepatocites. In the early stage of the disease there are multiple microabsccess in all the liver, (though is used the abscess term, the amebic abscesses are not real abscesses, since they contain few neutrophil, since they are constituted by liquefied hepatic cells).(2,3,4,5) In this stage, the patient is presented with high fever, abdominal pain superior right and enlarged liver with painful sensibility al tact. This stage sometimes is called hepatitis amebiana. With its progression, the microabsccess are joined to form abscesses but large. From the point of view macroscopic the abscesses are large, they are have an irregular wall and contain - " pus " - amebiana, that has the dye tipicamente brown reddish (similar to the anchoas paste) of the necrotic liver. there is trophozoites in the wall of the abscess.(3,4)

The patients can have one or several hepatic abscesses amebianos, some of they are very large, sometimes destroy an entire hepatic lobe, They contain opaque liquid, gray, yellow material; wall is fragile and fibrinous, the trophozoites they are in the periphery, In the center there is necrosis, fibrine but there is no neutrophilic infiltrates neither bacteria, The liver that surrounds to the abscess is edematous; The mortality in this complication is the 48% without treatment. The election treatment is the metronidazol for by intravenous or oral. It is not necessary the drainage of the abscess by surgical. (4,7,11)

Ultrastructure.- Studies by electron microscopy reveal degenerative changes in epithelial cells as trophozoites approach. This support the belief that trophozoites elaborate a cytolytic substance. The initial injury produced in the mucous of the colon and liver caused by the ameba is due to the direct harmful action. (6,10,11)

The breakthrough mechanisms of the amiba in the intestinal epithelium and liver are similar and they can be :

1. - mechanical Effect of the ameba

2. - necrotic Effect produced by cytolitic enzimes eliminated by the ameba.

So soon the ameba is near the cells and it produced an electrodenso material that could be cytolitic enzimes; (fig.7) The separation of the epithelial cells begins in the membrane basal and then in the unions intercelulares; furthermore are produced granules osmiophilic similar to the granules intramitochondrials dependent of the calcium. This provokes changes in the metabolism of the calcium, lost of calcium in the union and separation sites of the complex of union. (5,6)

The cells of the epithelium in touch with the ameba show shortening and disappearance of microvilli, edema of mitochondrias, dilated rer and absence of the terminal bar; When the trophozoite was identified in the thickness of the epithelium, it was observed that was destroying to the cells with those which was in touch. Furthermore the trophozoite was showing abundant lisosomales vesicles,they provoke effects membranous citolytics and they facilitate the breakthrough of the parasite. (5,6,7)

Conclussion:

We present one case of amebic abscess of the liver with clinicopathologic and ultrastructural analysis; seven photographs, they identify amebic morphology.


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