Estudo, ao microscópio óptico e eletrônico, do rim de caes natural e experimentalmente infectados com Leishmania (Leishmania) chagasi

Os autores estudam os rins de 4 cães infectados com Leishmania (Leishmania) chagasi. Dois animais (um macho e uma fêmea) naturalmente infectados foram sacrificados 18 meses após sua permanência no laboratório. Dois machos foram inoculados por via endovenosa, com lxlO6 promastigotas da cepa MHO/BR/70/BH46 e sacrificados após 18 meses e 2 anos, respectivamente. Em todos os animais os rins estavam lesados. As alterações encontradas foram: (1) glomerulonefrite mesangioproliferativa focal ou difusa, com pronunciada hipertrofia e hiperplasia das células mesangiais e com alargamento da matriz; (2) espessamento da membrana basal com depósitos eletrondensos; (3) nefrite intersticial intertubular crônica com exsudação plasmocitária intensa. (4) degeneração albuminosa dos túbulos renais. Baseados nos achados os autores discutem os prováveis mecanismos patogenéticos.

Chronic myocardial damage in experimental T. cruzi infection of a new world primate, Cebus sp. monkey

Eighteen Cebus apella monkeys, (juvenile and adult of both sexes) were inoculated five years ago, with three Trypanosoma cruzi strains (CA1, n = 10; Colombian, n=4 and Tulahuen, n=4), either by conjunctival or intraperitoneal route, once or repeatedly. Parasitological, hematological, serological, enzymatic, radiographic, electro and echocardiographic findings have been peviously published15 and they are similar to those observed in human pathology. The most frequent electrocardiographic alteration was right branch bundle block. Six animals, chosen at random, were sacrificed. Those sacrificed 20 to 25 months post-first inoculation showed focal accumuli of leukocytes with myocytolysis. Foci of diffuse interstitial fibrosis with mild infiltrate of leukocytes among fibers were observed in the animals sacrificed 36 to 47 months post-inoculation. No parasites were seen. The lesions were more prominent in the ventricular walls and the septum. The fact that the infiltrates were predominant in the animals sacrificed at a shorter time after first inoculation and that fibrosis was more severe in those sacrificed at a longer time suggests that there is a progression of the infiltrative lesions to fibrosis, with a leukocytic activity indicative of a chronic phase. These lesions are similar to those described in human chronic Chagas' disease. This would demonstrate that this model is useful in evaluating a progress in the knowledge of the pathogenesis which is still a controversial issue, immunology, immunogenesis and chemotherapeutic agents of the chronic and indeterminate phases of this disease.

Pathology of periportal fibrosis involution in human schistosomiasis

Optical and electron microscopical evidences of focal matrix degradation were frequently seen in liver sections of periportal fibrosis caused by schistosomiasis mansoni in man. The material came from 14 wedge hepatic biopsies taken from patients with chronic advanced hepatosplenic disease and undergoing operations for the relief of portal hypertension. Besides the presence of focal areas of rarefaction, fragmentation and dispersion of collagen fibers, the enlarged portal spaces also showed hyperplasia of elastic tissue and disarray of smooth muscle fibers following destruction of portal vein branches. Eggs were scanty in the tissue sections, and matrix degradation probably represented involuting changes related to the progressive diminution of parasite-related aggression, which occurs spontaneously with age or after cure by chemotherapy. The changes indicative of matrix degradation now described are probably the basic morphological counterpart of periportal fibrosis involution currently being documented by ultrasonography in hepatosplenic patients submitted to curative chemotherapy.

Patogênese da miocardite chagásica crônica: o papel de fatores autoimunes e microvasculares

A patogênese da miocardite chagásica crônica permanece incompletamente compreendida. Diferentes hipóteses têm sido propostas: (1) lesão direta do tecido pelo Trypanosoma cruzi;(2) teoria neurogênica; (3) reações imunológicas anti-miocárdio; e (4) doença microvascular. Apresentamos, no presente trabalho, uma hipótese alternativa. Acreditamos que o desenvolvimento da miocardite está relacionado à necrose celular focal progressiva e acumulativa, associada à fibrose intersticial reparativa e reativa e hipertrofia miocitária circunjacente. Esses processos seriam iniciados e perpetuados por fatores autoimunes e alterações na microcirculação do miocárdio. Esse mecanismo fisiopatogênico teria possíveis implicações em futuras estratégias terapêuticas no tratamento do paciente chagásico crônico visando otimizar o tratamento médico e auspiciosamente melhorar o prognóstico.

Experimental paracoccidioidomycosis in hamster: transmission electron microscopy of inoculation site lesion

Interaction between Paracoccidioides brasiliensis (Pb) and inflammatory cells in hamster testis was studied sequentially by transmission electron microscopy. In early lesions (six hours after inoculation), polymorphonuclear neutrophils (PMNs) were the major and mononuclear cells and eosinophils were the minor constituents of the inflammatory cells. PMNs were later replaced by mononuclear cells. Viable Pb cells were phagocytosed or surrounded by inflammatory cells. Preserved Pb cells usually had broad host-parasite interphases, whereas dying ones had narrow interphases. The outer layer of the fungus wall was sometimes broken by PMN in some focal points, broken pieces being peeled off and phagocytosed. Small Pb cells were uninuclear, and were often related to broad interphase. Large Pb cells were multinucleated with irregularly shaped wall, and sometimes had lomasome and/or myelin like structures. Different interaction patterns of Pb with inflammatory cells may be due to functionally different host cell flow to the inoculation site or due to the age of Pb cells or both.

Histopatologia da forma localizada de leishmaniose cutânea por Leishmania (Leishmania) amazonensis

São descritas as alterações microscópicas presentes na forma localizada (ulcerada) da Leishmaniose cutânea produzida por Leishmania (Leishmania) amazonensis. Nesse tipo de manifestação, menos conhecido do que a forma anérgica ou difusa devida ao mesmo agente, as lesões são clinicamente idênticas às de leishmaniose cutânea causada por espécies outras de Leishmania, pertencentes ao subgênero Viannia. Na infecção localizada por L. (L.) amazonensis, entretanto, há um aspecto peculiar, só recentemente conhecido, ou seja, cerca de 50% dos indivíduos atingidos não reagem ao teste de Montenegro. A principal característica histológica observada foi a acumulação na derme, quase sempre focal, de numerosos macrófagos contendo no citoplasma um grande vacúolo cheio de amastigotas. O quadro é semelhante ao da forma difusa, porém sem o aspecto histiocitomatóide, próprio da última. Afora esses grupos de macrófagos, vêem-se também, na forma localizada, muitas células mononucleares da inflamação, principalmente plasmócitos e macrófagos não parasitados. Os acúmulos de macrófagos com amastigotas, quando volumosos, podem sofrer necrose na parte central; os parasitos, contidos nas células, são destruídos com elas ou liberados, e sua eliminação através da úlcera deve contribuir para a cura do processo. Esse tipo de necrose nunca foi descrito em casos da forma difusa. Não houve grande diferença, no quadro histológico, entre pacientes Montenegro-negativos e positivos. Apenas em alguns casos, do grupo Montenegro-positivo, havia granulomas formados por histiócitos epitelióides sem parasitos. Quanto à persistência das células com parasitos nas lesões, observou-se que aos seis meses ou mais de evolução, em ambos os grupos, ainda estavam elas presentes. Tal achado não é comum na leishmaniose tegumentar por L. (V.) braziliensis.

Paracoccidioidomycosis associated with acquired immunodificiency syndrome: report of seven cases

We report the clinical findings and evolution of seven patients (five men and two women), the majority of them intravenous drug users, with paracoccidioidomycosis associated to acquired immunodeficiency syndrome (AIDS). In four of the patients the paracoccidioidomycosis was restricted to the lung and in the three others was generalized with cutaneous involvement. Only two of them had lived recently in rural area, an indication of the possible reactivation of latent focal infection in the other five patients. The recognition of the role of cell-mediated immunity in host defense against Paracoccidioides brasiliensis leds to the prediction of a growing occurrence of the paracoccidioidomycosis-AIDS association in areas that are endemic for these diseases.

FETO-PLACENTARY PATHOLOGY IN HUMAN PARVOVIRUS B19 INFECTION

In view of the scarce references concerning the histological data in congenital parvovirus human B19 infection, we intend to provide a description of the pathological features observed in six autopsies.The virus was detected by DNA hybridization (ISH-DBH),PCR and electronmicroscopy (EM) in paraffin-embedded feto-placentary tissues.These cases constitute a subset from 86 Non Immunologic Hydrops Fetalis (NIHF) cases, in which a systemic complex of inflammatory/degenerative lesions of unknown etiology was visualized by optical microscopy. In one case a syphilitic process was detected, typefying a double infection. All fetuses showed a similar pathology - hydrops, hepato-splenomegaly, lung hypoplasia and erythroblastemia, the specific histological feature being the presence of intranuclear inclusions in the erythroid progenitors, in the erythropoietic visceral tissue and in blood marrow. Complex cardiopathy allied to abnormal lung lobulation and polisplenia were observed once; in 2 cases endocardial fibroelastosis was diagnosed. The pulmonary lesions were represented by dysmaturity allied to interstitial mononuclear infiltration. The hepatic consisted of cholestasis, portal fibrosis, canalicular proliferation, hemossiderosis, focal necroses and giant cell transformation. The central nervous system lesions were predominantly anoxic although the autolysis impaired a correct diagnosis.

Experimental dermatophytosis in hamsters inoculated with Trichophyton mentagrophytes in the cheek pouch

This study presents the results of T. mentagrophytes inoculation in the cheek pouch of the hamster, an immunologically privileged site. Forty two animals were used: 21 inoculated with 10(6) fungi in the cheek pouch (group 1) and 21 inoculated initially with 10(6) fungi in the foot pad and 15 days later in the cheek pouch, with the same amount of fungi (group 2). Animals were sacrificed at 20 hours, 3, 7, 14, 30, 60, and 120 days; samples from inoculated cheek pouch, and foot pads submitted to the foot pad test (FPT), were collected. Independent of group and time of evolution of infection, animals did not develop delayed hypersensitivity evaluated through the FPT. The pre-inoculation of fungi in the foot pad did not change the morphology of lesions induced in the cheek pouch. Therefore, in animals of group 1 and 2, the introduction of the fungus in the cheek pouch resulted in focal lesion composed of a sterile acute inflammatory infiltrate, with abscess formation that evolved to a macrophagic reaction, and later to resolution even in the absence of immune response detectable by FPT. Our results indicate that in spite of the important role of the immune response in the spontaneous regression of dermatophytosis, other factors are also an integral part in the defense against this fungal infection.

Clinical patterns and seasonal trends in respiratory syncytial virus hospitalizations in São Paulo, Brazil

The respiratory viruses are recognized as the most frequent lower respiratory tract pathogens for infants and young children in developed countries but less is known for developing populations. The authors conducted a prospective study to evaluate the occurrence, clinical patterns, and seasonal trends of viral infections among hospitalized children with lower respiratory tract disease (Group A). The presence of respiratory viruses in children's nasopharyngeal was assessed at admission in a pediatric ward. Cell cultures and immunofluorescence assays were used for viral identification. Complementary tests included blood and pleural cultures conducted for bacterial investigation. Clinical data and radiological exams were recorded at admission and throughout the hospitalization period. To better evaluate the results, a non- respiratory group of patients (Group B) was also constituted for comparison. Starting in February 1995, during a period of 18 months, 414 children were included- 239 in Group A and 175 in Group B. In Group A, 111 children (46.4%) had 114 viruses detected while only 5 children (2.9%) presented viruses in Group B. Respiratory Syncytial Virus was detected in 100 children from Group A (41.8%), Adenovirus in 11 (4.6%), Influenza A virus in 2 (0.8%), and Parainfluenza virus in one child (0.4%). In Group A, aerobic bacteria were found in 14 cases (5.8%). Respiratory Syncytial Virus was associated to other viruses and/or bacteria in six cases. There were two seasonal trends for Respiratory Syncytial Virus cases, which peaked in May and June. All children affected by the virus were younger than 3 years of age, mostly less than one year old. Episodic diffuse bronchial commitment and/or focal alveolar condensation were the clinical patterns more often associated to Respiratory Syncytial Virus cases. All children from Group A survived. In conclusion, it was observed that Respiratory Syncytial Virus was the most frequent pathogen found in hospitalized children admitted for severe respiratory diseases. Affected children were predominantly infants and boys presenting bronchiolitis and focal pneumonias. Similarly to what occurs in other subtropical regions, the virus outbreaks peak in the fall and their occurrence extends to the winter, which parallels an increase in hospital admissions due to respiratory diseases.

Infectious agents in coronary atheromas: a possible role in the pathogenesis of plaque rupture and acute myocardial infarction

In this review we report our recent findings of histopathological features of plaque instability and the association with Mycoplasma pneumoniae (MP) and Chlamydia pneumoniae (CP) infection, studying thrombosed coronary artery segments (CAS) of patients who died due to acute myocardial infarction. Vulnerable plaques are known to be associated with fat atheromas and inflammation of the plaque. Here we demonstrated that vulnerability is also related with focal positive vessel remodeling that maintains relatively well preserved lumen even in the presence of large atheromatous plaques. This phenomena may explain why the cinecoronariography may not detect large and dangerous vulnerable plaques. Greater amount of these bacteria in vulnerable plaques is associated with adventitial inflammation and positive vessel remodeling: the mean numbers of lymphocytes were significantly higher in adventitia than in the plaque, good direct correlation was obtained between numbers of CD20 B cells and numbers of CP infected cells in adventitia, and between % area of MP-DNA in the plaque and cross sectional area of the vessel, suggesting a cause-effect relationship. Mycoplasma is a bacterium that needs cholesterol for proliferation and may increase virulence of other infectious agents. In conclusion, co-infection by Mycoplasma pneumoniae and Chlamydia pneumoniae may represent an important co-factor for plaque instability, leading to coronary plaque thrombosis and acute myocardial infarction, since larger amount of these bacteria strongly correlated with histological signs of more vulnerability of the plaque. The search of CMV and Helicobacter pilori in these tissues resulted negative.