Laser therapy reduced the inflammatory reaction, induced increased collagen deposition and a greater proliferation of myofibroblasts in experimental cutaneous wounds.

Schistosoma mansoni infection invariably results in liver fibrosis of the host. This fibrosis may be represented by small focal areas of chronic inflammation and excess extracellular matrix deposited in periovular granulomas, distributed in variable numbers at the periphery of the portal vein system. This is the outcome of 90% of the infected population in endemic areas. Conversely, a minority of infected individuals develop extensive disease with numerous granulomas along the entire extension of the portal spaces. This latter situation is mainly dependent on special hemodynamic changes created by a heavy worm load, with the subsequent production of numerous eggs and represents a severe form of a peculiar chronic hepatopathy. Thus, host-parasite interactions in schistosomiasis help us to understand a number of important features of liver fibrosis: its initiation and regulation, the significance of accompanying vascular changes, the dynamics of fibrosis formation and regression with antiparasitic treatment; host genetic and immunological contributions, and the pathophysiology of portal hypertension.

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Advanced schistosomiasis produces in man one of the most characteristic gross picture presentation of hepatic pathology. On the cut surface of the liver this lesion appears as whitish fibrous plaques replacing portal spaces on a background of normal looking hepatic parenchyma (Fig. 1C, D). Exactly one century ago, Symmers (1904) classically described this picture after performing autopsies in Egypt. It represents the anatomical counterpart of the clinical condition known as hepatosplenic schistosomiasis. A cursory gross and microscopic examination of the lesion will reveal important clues about its pathogenesis. It can then be noted that the lesion resulted from the deposition of numerous schistosome eggs along the periportal tissues, which provoked chronic granulomatous inflammation with consequent fibrous expansion of the portal spaces and intrahepatic portal vein obstruction. The parenchyma usually maintains its normal architecture, in a good correlation with the preservation of the normal hepatic function, as usually exhibited by the patients. The presence of numerous eggs points to the pathogenetic importance of worm load. Thus, schistosomal hepatopathy seems a good example of a straightforward condition, with a simple, characteristic, and understandable pathology.Although these main lines mentioned above are correct, they say little about the complexities that this unique type of chronic hepatopathy discloses when more closely and properly investigated. A closer view of its physiopathology will reveal several points of interests that are usually overlooked, but that are important for the understanding of the disease in patients and so are worth discussing here. Schistosomal hepatopathy represents a special type of a chronic liver disease. Its pathology contains unique features, one of the most important refers to its vascular changes, which differs from those found in cirrhosis, and are key factors for the understanding of the fundamental pathogenesis and the clinical potential for evolution presented by hepatosplenic schistosomiasis.

The indeterminate phase of Chagas' disease is defined as the prolonged period of clinically silent infection that follows the phase of acute primary infection with Trypanosoma cruzi. The dog is the only experimental animal model in which the indeterminate phase progresses to the late phase of severe, chronic myocarditis. This report describes the cardiac histologic and ultrastructural findings in dogs that survived the acute phase of infection with T. cruzi, becoming clinically and electrocardiographically normal for up to 3.5 years, while maintaining positive serologic test results during this period of time. Most of the myocardium appeared morphologically normal; however, small foci of mild, chronic myocarditis were present, with interstitial edema, mild fibrosis, and infiltration by lymphocytes, macrophages, and plasma cells. No microvascular lesions and no areas of close contact between immune effector cells and endothelial cells or cardiac myocytes were present. These findings were in sharp contrast to those observed in the canine model during the acute infection with T. cruzi. In this model, acute myocyte damage and lesions in the microcirculation, including fibrin microthrombi, were associated with close contacts between immune effector cells and myocytes or endothelial cells. Focally inflamed interstitial tissue showed increased deposition of amorphous and collagenous extracellular matrix as well as evidence of breakdown of collagen. The features of the inflammatory cells in the indeterminate phase of Chagas' disease were interpreted as indicating a self-limited cycle of focal inflammatory changes, with modulation and suppression of cell-mediated immune responses. Thus, we consider the indeterminate phase of Chagas' disease to be a stage of host-parasite equilibrium rather than a process of progressive damage.

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Cães jovens infectados pelo Trypanosoma cruzi desenvolveram a fase aguda da infecção e foram estudados durante o 7º até o 50º dia por métodos morfológicos, parasitológicos, imunológicos e eletrocardiográficos. ocorreu intensa miocardite que se iniciava nos átrios e se propagava aos ventrículos e, quando plenamente desenvolvida, predominava no átrio direito, na metade direita do septo interventricular e na parede livre do ventrículodireito. As alterações eletrocardiográficas foram progressivas e revelavam o progressivo e predominante comprometimento atrial, mas a interferência com a propagação do estímulo (bloqueio) só apareceu nas fases terminais, coincidente com a presença de inflamação e necrose ao longo do tecido de condução. Quinze cães foram submetidos a tratamento específico e em alguns destes as modificações anátomo-patológicas e eletrocardiográficas representaram uma reversão progressiva das lesões observadas antes. Dez animais evoluíram para a fase crônica indeterminada da infecção, três deles após tratamento, e foram acompanhados por períodos de oito meses a três anos, sem que nenhum desenvolvesse sinais de insuficiência cardíaca congestiva. As alterações eletrocardiográficas observadas nestes casos foram inespecíficas e algumas arritmias apareceram transitoriamente. No sistema excito-condutor foram encontradas lesões focais de fibrose, esclero-atrofia e infiltração adiposa, as quais foram interpretadas como seqüelas deixadas pela fase aguda. A miocardite encontrada foi focal e discreta. Foi examinado para complementação o material de um caso de forma crônica cardíaca no cão, o qual exibiu miocardite difusa com fibrose focal e intersticial e sinais de atividade do processo inflamatório, além de bloqueio de ramo direito e hemibloqueio anterior esquerdo. Assim, o modelo canino da doença de Chagas reproduz todas as fases da cardiopatia, tal como aparece no homem, sendo que as formas crõnicas sintomáticas são de reprodução experimental imprevisível. O presente trabalho objetivou caracterizar os aspectos da patologia da doença de Chagas no cão, tentar as suas correlações eletrocardiográficas, os seus aspectos evolutivos, com a finalidade de fornecer elementos para estudos futuros com o referido modelo experimental.
Young dogs experimentally infected with Trypanosoma cruzi developed acute disease and were studied by pathologic, immunologic, parasitologic and eletrocardiographic methods. The main lesion was an acute myocarditis that began in the atria and propagated through the septum toward the ventricles and, when fully developed, predominated in the right atrium, the right half of the ventricular septum and the free wall of the right ventricle. ECG changes were progressive and reflected the predominant atrial involvement. Cardiac blocks appeared only at the terminal stages and coincided with severe inflammation and necrosis along the A-V conducting tissue. Specific treatment made in 15 dogs with severe acute disease frequently reversed both the histological and ECG changes. Ten animals went into a chroni...