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Lechiguana is a disease of cattle caused by an interaction between Dermatobia hominis warble and the bacteria Manheimia granulomatis. It is characterized by subcutaneous swellings that grow rapidly and result in death after 3 to 8 months. The objective of this paper was to investigate some vascular and fibrogenic changes of the disease at different lesion stages by histochemical and immunohistochemical techniques. A peculiar histopathological aspect observed during a proliferative phase (before treatment) was the intense vasculitis, described as degenerative and fibro-proliferative, expressed by the oncogene p53, possibly caused by the presence of bacteria in close contact with enthotelial cells, along with dense accumulations of lymphoid cells around venules. The synthesis of collagen fibers during the development of Lechiguana lesions assume a structural aspect of star arrangement with fiber radiation centers that gradually interconnect to design the Extracellular Matrix (ECM) framework, seen by Confocal Laser Scanning Microscopy (CSLM). Angiogenesis was the most characteristic finding in both proliferative and regressive stages as seen by the immunohistochemical expression of cytoskeleton proteins and von Willebrand (Factor VIII-Related Antigen). Additionally, in all tissues samples, active ECM elements like Metalloproteinases (MMPs), Tissue Inhibitors Metalloproteinases (TIMP) and Fibronectin (FN) were mainly associated to vessels structures. The extraordinary regression of exuberant granulation tissue after treatment is undoubtedly associated to the maintenance of the vascular components observed during the regressive phase.

Objectives To describe clinical presentation and results of diagnostic and therapeutic procedures in seven children from an epidemic of panuveitis in the Brazilian Amazonia, as well as environmental analysis and etiological aspects involved. Methods Patients underwent full pediatric and ophthalmic examinations, B-scan, ultrasound biomicroscopy, and serological tests. Ocular samples were thoroughly analyzed, including two enucleation specimens. Environmental investigation encompassed water, soil, and river fauna. Results All patients had bathed in the waters of a regional river, the Araguaia. Six of them presented with intermediate uveitis, with snowbanking. Five had cataract and four showed inferior endothelial opacity, with localized anterior synechiae. One showed total leukoma, with flat anterior chamber. Only two had active uveitis, one of them with anterior chamber nodule. Serology revealed high prevalence of anti-Toxocara canis immunoglobulin G (IgG) antibodies. In three cases, vitreous and lens samples disclosed spicules of freshwater sponges Drulia uruguayensis and D. ctenosclera, also detected in the waters of the river. Conclusion Freshwater sponge spicules could be potential new etiological agents of ocular pathology, but further studies are needed, considering the heterogeneity of the ocular lesions and results of serological and environmental studies.

In life cycle of Angiostrongylus costaricensis, veronicellidae mollusks participate as the invertebrate host while rodents as the main vertebrate host. The current work shows a sequential larval development of A. costaricensis in Sarasinula marginata, individually killed and digested from day 1 to 43, post infection. Some larvae, recovered from sedimentation, were submitted to selective staining after paraffin embedded or inclusion in JB-4 to study inner structures. As control, four slugs were used, two killed at the beginning of infection and the others at the end of the experiment. At day 2 post infection, larvae were motionless and thick, presenting initial retention of granules. At day 4, L2 were detected, persisting until 43 days post infection. Larvae L2 displayed a large amount of granules rich in lipids and carbohydrates through its overall body, with more accumulation at the medial third corresponding to the esophagus–intestine transition site. Lipid granules, the main energetic source, were located at the basal and apical regions of intestinal cells. Both L1 and L3 presented bilateral alae, which is also common in other nematodes. Transition forms between L2 to L3 molts were also observed.

Schistosomiasis, a chronic disease with considerable social impact, is an important health problem in many countries. To investigate the possible use of immunomodulators as coadjuvants in the treatment of chronic Schistosoma mansoni infection, we evaluated the effect of dexamethasone on histological, hematological, and biochemical parameters that reflect disease severity and morbidity. Animals treated from the first day or after 35 days of infection, were analyzed. In both groups, dexamethasone: (1) induced a decrease in the number of granulomas in hepatic tissue without affecting the alanine aminotransferase profile, (2) reduced splenomegaly and hepatomegaly associated with disease, and (3) improved hemoglobin concentration, hematocrit values and reduced the percentage of reticulocytes, preventing the development of anemia that occurs in the chronic phase of infection. These data suggest that treatment with dexamethasone results in a mild course of murine schistosomiasis and point to this drug as a promising agent to complement S. mansoni specific treatment.

We previously reported that portal veins from mice infected with male Schistosoma mansoni exhibited an increased reactivity to 5-hydroxytryptamine (5-HT). Here, we extended our observations to mice infected by both male and female worms and we further investigated another constrictor agent and the mechanism(s) responsible for the enhanced maximal contraction ( E(max)). Bisexual infection increased the E(max) of 5-HT (from 0.66+/-0.06 mN.s to 1.56+/-0.38 mN.s), in a similar way to the unisexual (male) infection. Infection with male worms increased portal vein reactivity to acetylcholine, as revealed by a higher E(max) (1.03+/-0.2 mN.s) in relation to non-infected control animals ( E(max)= 0.54+/-0.08 mN.s). Sarcoplasmic/endoplasmic reticulum Ca(2+)-ATPase (SERCA) inhibition with 100 nM thapsigargin reduced the E(max) of 5-HT by 35% in both tissues, discharging a deficiency of SERCA pump in infected animals. In contrast, the number of voltage-dependent Ca(2+) channels (L-type) was higher in portal veins from infected than non-infected control mice. Inhibition of Ca(2+)-activated chloride channels (Cl(Ca)) with 10 micro M niflumic acid reduced the E(max) of 5-HT in portal veins more from infected than non-infected animals (remaining tension = 60.9+/-2.2% and 70.4+/-2.3%, respectively). Histopathological analysis revealed an increased content of collagen and elastin in portal veins from male S. mansoni-infected mice, compatible with an increased intraluminal pressure. In conclusion, male S. mansoni altered portal vein physiology, increasing the E(max) of two vasoconstrictors, possibly by increasing membrane depolarisation through a more effective opening of Cl(Ca) channels, with calcium entering through L-type Ca(2+) channels.

To compare the sequential evolution of lesions developed by resistant (A/Sn) and susceptible (B10.A) mice to Paracoccidioides brasiliensis infection we inoculated a virulent isolate of the fungus and collected the pancreas/peripancreatic omentum monthly (from 1 to 6 months) post infection. After fixation, tissue sections were stained by conventional methods for light microscopy to investigate the cellular composition, the extracellular matrix (ECM) patterns and the morphology of the yeasts in the lesions. In both strains, the fungal lesions were localized mostly in the omentum; a few lesions in the pancreatic parenchyma were observed, mostly in B10.A mice. In both strains, macrophages and plasmocytes were the predominant cells in all lesions, followed by neutrophils (PMN) and macrophages transformed into giant and epithelioid cells. Remarkable differences were observed between resistant and susceptible mice, specially related to the ECM structure of the granulomatous lesions. In A/Sn mice, from the 1st month on, the coexistence of two types of lesions was observed: one type showed a well-defined encapsulated nodule, constituted mainly of type I collagen. Neutrophils were abundant in areas of massive fungal destruction and few viable yeasts were observed. The other type showed residual characteristics, with sparse collagen deposits and presence of xantomatous-like macrophages, containing degenerated fungi. Such residual lesions predominated after the 2nd month and were the only type observed from the 4th month on, indicating the control of the infection. In B10.A mice, on the contrary, only one type of lesion was observed, showing less tendency to encapsulation and the formation of multiple small granulomatous foci, individualized by reticular type III collagen fibers. There were many plasmocytes in the periphery and large numbers of budding yeasts, with no evidence of fungal destruction. In the course of the infection the lesions progressively increased in number and size. Altogether, the comparative histopathological analysis demonstrates the influence of the genetic pattern of the host on the lesions developed by resistant and susceptible mice to P. brasiliensis infection.

An increasing number of cases of abdominal angiostrongyliasis have recently been diagnosed in southern Brazil. A comparative study of 19 confirmed cases and 15 suspected cases was undertaken to review the anatomo-pathology of the disease and to establish histopathological criteria for its diagnosis. The results were similar in both groups, except for the identification of the worm in the confirmed cases. Macroscopic features comprised two types: a predominant thickening of the intestinal wall (pseudo-neoplastic pattern) and a congestive necrotic lesion (ischemic-congestive pattern). Microscopically, three fundamental histopathological findings were detected: (1) a massive infiltration of eosinophils in all layers of the intestinal wall, (2) a granulomatous reaction and (3) eosinophilic vasculitis affecting arteries, veins, lymphatics and capillaries. We conclude that observation of this histopathological triplet excludes other causes of "eosinophilic gastroenteritis" and establishes the diagnosis of probable abdominal angiostrongyliasis.