120 resultados para PATHOLOGICAL GAMBLERS
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PURPOSE: In placentas from uncomplicated pregnancies, Hofbauer cells either disappear or become scanty after the fourth to fifth month of gestation. Immunohistochemistry though, reveals that a high percentage of stromal cells belong to Hofbauer cells. The aim of this study was to investigate the changes in morphology and density of Hofbauer cells in placentas from normal and pathological pregnancies. METHODS: Seventy placentas were examined: 16 specimens from normal term pregnancies, 10 from first trimester's miscarriages, 26 from cases diagnosed with chromosomal abnormality of the fetus, and placental tissue specimens complicated with intrauterine growth restriction (eight) or gestational diabetes mellitus (10). A histological study of hematoxylin-eosin (HE) sections was performed and immunohistochemical study was performed using the markers: CD 68, Lysozyme, A1 Antichymotrypsine, CK-7, vimentin, and Ki-67. RESULTS: In normal term pregnancies, HE study revealed Hofbauer cells in 37.5% of cases while immunohistochemistry revealed in 87.5% of cases. In first trimester's miscarriages and in cases with prenatal diagnosis of fetal chromosomal abnormalities, both basic and immunohistochemical study were positive for Hofbauer cells. In pregnancies complicated with intrauterine growth restriction or gestational diabetes mellitus, a positive immunoreaction was observed in 100 and 70% of cases, respectively. CONCLUSIONS: Hofbauer cells are present in placental villi during pregnancy, but with progressively reducing density. The most specific marker for their detection seems to be A1 Antichymotrypsine. It is remarkable that no mitotic activity of Hofbauer cells was noticed in our study, as the marker of cellular multiplication Ki-67 was negative in all examined specimens.
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The epidemiology, clinical picture and pathology of an outbreak of urolithiasis in cattle in southern Brazil are described. The disease occurred in August 1999 in a feedlot beef cattle herd. Five out of 1,100 castrated steers were affected. Clinical signs included colic and ventral abdominal distension. White, sand-grain-like mineral deposits precipitated on the preputial hairs. Affected cattle died spontaneously 24-48 hrs after the onset of the clinical signs. Only one animal recovered after perineal urethrostomy. Necropsy findings included calculi blocking the urethral lumen of the distal portion of the penile sigmoid flexure, urinary bladder rupture with leakage of urine into the abdominal cavity and secondary fibrinous peritonitis. Daily water intake was low since water sources were scarce and not readily available. The animals were fed rations high in grains and received limited amounts of roughage. Biochemical analysis revealed that the calculi were composed of ammonium phosphate. A calcium-phosphorus imbalance (0.4:0.6) was detected in the feedlot ration. For the outbreak, it is suggested that contributing factors to urolith formation include insufficient fiber ingestion, low water intake and high dietary levels of phosphorus. No additional cases were observed in that feedlot after preventive measures were established. Similar dietary mismanagement in fattening steers has been associated with obstructive urolithiasis in feedlot beef cattle in other countries.
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Ipomoea carnea subsp. fistulosa, aguapei or mandiyura, is responsible for lysosomal storage in goats. The shrub contains several alkaloids, mainly swansonine which inhibits lysosomal α-mannosidase and Golgi mannosidase II. Poisoning occurs by inhibition of these hydrolases. There is neuronal vacuolation, endocrine dysfunction, cardiovascular and gastrointestinal injury, and immune disorders. Clinical signs and pathology of the experimental poisoning of goats by Ipomoea carnea in Argentina are here described. Five goats received fresh leaves and stems of Ipomoea. At the beginning, the goats did not consume the plant, but later, it was preferred over any other forage. High dose induced rapid intoxication, whereas with low doses, the course of the toxicosis was more protracted. The goats were euthanized when they were recumbent. Cerebrum, cerebellum, medulla oblongata, pons and colliculi, were routinely processed for histology. In nine days, the following clinical signs developed: abnormal fascies, dilated nostrils and abnormal postures of the head, cephalic tremors and nystagmus, difficulty in standing. Subsequently, the goats had a tendency to fall, always to the left, with spastic convulsions. There was lack in coordination of voluntary movements due to Purkinje and deep nuclei neurons damage. The cochlear reflex originated hyperreflexia, abnormal posture, head movements and tremors. The withdrawal reflex produced flexor muscles hypersensitivity at the four legs, later depression and stupor. Abnormal responses to sounds were related to collicular lesions. Thalamic damage altered the withdrawal reflex, showing incomplete reaction. The observed cervical hair bristling was attributed to a thalamic regulated nociceptive response. Depression may be associated with agonists of lysergic acid contained in Ipomoea. These clinical signs were correlated with lesions in different parts of the CNS.
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In Brazil, the consumption of Sida carpinifolia by livestock has been associated with neurological diseases linked to lysosomal storage disorders. This paper describes the pathological findings in two caprine fetuses from dams that were experimentally poisoned with S. carpinifolia. The goats were orally dosed with 10 and 13g/kg of a paste of green chopped S. carpinifolia for 30 days and were observed for an additional 15 days period after the last dosage with the plant; thereafter they were euthanized and necropsied. The dams showed only slight clinical signs. The study also includes the findings in one bovine fetus from a naturally S. carpinifolia poisoned cow which showed mild incoordination, generalized tremors, staggering, and frequent falls. The cow was euthanized and necropsied. While there were no significant histopathological changes in the goats, in the cow vacuolation of Purkinje neurons of the cerebellum, pancreatic acinar cells, and thyroid follicular cells were observed. The main microscopic changes observed in the caprine and bovine fetuses were vacuolation in the epithelium of renal tubules, thyroid follicular cells, and Purkinje neurons of the cerebellum. Transmission electron microscopy of sections from CNS of the cow and its fetus revealed vacuoles containing fine granular material surrounded by membrane. Lectin-histochemistry of CNS sections from goat fetuses marked lightly to sWGA lectins, WGA, and Con-A.
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This study reports on changes in the number of somatostatin-like immunoreactive (SOM-LI) endocrine cells in the porcine descending colon, caused by chemically driven inflammation, axotomy and proliferative enteropathy (PE). The distribution pattern of SOM-LI endocrine cells has been studied using the routine single-labelling immunofluorescence technique. Semi-quantitative evaluation of the number of the SOM-immunostained endocrine cells within the mucosal layer of the porcine descending colon has been based on counting of all endocrine cells immunoreactive to SOM per unit area (0,1 mm²). Under physiological conditions the number of SOM-LI endocrine cells has been shown to constitute 3,30±0,22. All applied pathological processes resulted in changes in the SOM-like immunoreactivity, which varied in particular processes studied. The number of SOM-LI endocrine cells increased to 6,28±0,31 and 4,43±0,35 during chemically driven inflammation and proliferative enteropathy, respectively, and decreased to 1,17%±0,16 after axotomy. The obtained results suggest that SOM-LI endocrine cells may participate in various pathological states within porcine descending colon and their functions probably depend on the type of pathological factor.
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Influenza A virus (IAV) is a respiratory pathogen of pigs and is associated with the porcine respiratory disease complex (PRDC), along with other respiratory infectious agents. The aim of this study was to diagnose and to perform a clinic-pathological characterization of influenza virus infection in Brazilian pigs. Lung samples from 86 pigs in 37 farrow-to-finish and two farrow-to-feeder operations located in the States of Minas Gerais, São Paulo, Paraná, Rio Grande do Sul, Santa Catarina, and Mato Grosso were studied. Virus detection was performed by virus isolation and quantitative real time reverse-transcription PCR (qRT-PCR). Pathologic examination and immunohistochemistry (IHC) were performed in 60 lung formalin-fixed paraffin-embedded tissue fragments. Affected animals showed coughing, sneezing, nasal discharge, hyperthermia, inactivity, apathy, anorexia, weight loss and growth delay, which lasted for five to 10 days. Influenza virus was isolated from 31 (36.0%) lung samples and 36 (41.9%) were positive for qRT-PCR. Thirty-eight (63.3%) lung samples were positive by IHC and the most frequent microscopic lesion observed was inflammatory infiltrate in the alveoli, bronchiole, or bronchi wall or lumen (76.7%). These results indicate that influenza virus is circulating and causing disease in pigs in several Brazilian states.
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This paper describes an outbreak of chronic Senecio spp. poisoning in grazing sheep in Rio Grande do Sul, Brazil, causing the death of 10 out of 860 adult sheep. Eight sick ewes were euthanized and necropsied. Cattle from this farm were also affected. Clinical signs included progressive weight loss, apathy and photosensitization. Four out of seven tested sheep had increased gamma-glutamyl transferase serum activity and two of them presented serum elevation of alkaline phosphatase. At necropsy, three out of eight ewes presented slightly irregular toughened livers with multifocal nodules, two out of eight ewes had a whitish liver with thickened fibrotic Glisson's capsule partially adhered to the diaphragm, and three out of eight ewes had smooth and grossly normal livers. Necropsy findings attributed to liver failure included hydropericardium (7/8), ascites (5/8), icterus (2/8), hydrothorax (1/8), and edema of mesentery (1/8). The main hepatic histological findings that allowed the establishment of the diagnosis were megalocytosis, proliferation of bile ducts and fibrosis. Spongy degeneration was observed in the brains of all eight necropsied sheep and was more severe at the cerebellar peduncles, mesencephalon, thalamus, and pons. These are suggested as the portions of election to investigate microscopic lesions of hepatic encephalopathy in sheep with chronic seneciosis. The diagnosis of Senecio spp. poisoning was based on epidemiology, clinical signs, laboratory data, necropsy and histological findings.
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Fatal Human herpesvirus 1 (HHV-1) was diagnosed in 12 captive marmosets (Callithrix jacchus and Callithrix penicillata) from metropolitan region of São Paulo, São Paulo State. Clinical signs were variable among the cases, but most affected marmosets presented signs associated with viral epithelial replication: oral, lingual and facial skin ulcers and hypersalivation, and viral replication in the central nervous system: prostration, seizure and aggressive behavior. Consistent microscopic findings were diffuse mild to severe nonsuppurative necrotizing meningoencephalitis with gliosis, vasculitis and neuronal necrosis. Additionally, in the brain, oral cavity, skin, adrenal gland and myoenteric plexus intranuclear inclusion bodies were present. Immunohistochemistry confirmed the presence of the HHV-1 antigen in association with lesions in the brain, oral and lingual mucosa, facial skin, adrenal gland and myoenteric plexus. HHV-1-specific polymerase chain reaction (PCR) analysis of the brain was carried out and the virus was detected in 7/8 infected marmosets. It is concluded that HHV-1 causes widespread fatal infection in marmosets.
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Abstract:Trematodes belonging to the family Eucotylidae, including Tanaisia(Paratanaisia)bragaiSantos, 1934are parasites of the kidney and ureter that affect several species of domestic and wild birds. Tanaisia bragaiis considered a low pathogenic parasite, but high worm burdens may determine clinical complications, including signs of apathy, weight loss, diarrhea and death. This paper describes the first report of infection by T. bragai in peacocks (Pavo cristatus), which constitutes a new host record and offers data on the lesions associated to this parasitism, although the degree of pathogenicity and parasite load may be considered mild. These birds did not exhibit clinical signs of parasitism. The macroscopic exam revealed discreet yellow spots on the liver. In the histological sections of the kidney, specimens of T. bragai were found in the collecting ducts, which were markedly dilated, with a thickened wall. Other findings included a mild inflammatory reaction in the wall of the ducts (but sometimes absent), flattening of lining epithelial cells and small, multifocal points of calcification around the collecting ducts. The microscopic examination of the parasites revealed trematodes with an elongated body, well-developed sub terminal oral sucker, pharynx present, short esophagus, cecum somewhat undulating or not, with blind end, testes symmetrical, equatorial, irregular in shape or slightly lobed, vitelline fields extending in both pre-ovarian and post ovarian fields, uterus very long, intercecal or sometimes overlapping the cecum and containing large quantities of eggs. The present findings suggest the need for further diagnostic studies on the prevalence of this trematode in peacocks as well as pathologic studies for the determination of the potential pathogenicity of this parasite in this species of bird. Moreover, infected peacocks could serve as carriers of T. bragai to be transferred to other bird species, thereby contributing to the dispersion of the parasite.
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The sarcoplasmic reticulum (SR) Ca2+-ATPase (SERCA2a) is under the control of an SR protein named phospholamban (PLN). Dephosphorylated PLN inhibits SERCA2a, whereas phosphorylation of PLN at either the Ser16 site by PKA or the Thr17 site by CaMKII reverses this inhibition, thus increasing SERCA2a activity and the rate of Ca2+ uptake by the SR. This leads to an increase in the velocity of relaxation, SR Ca2+ load and myocardial contractility. In the intact heart, ß-adrenoceptor stimulation results in phosphorylation of PLN at both Ser16 and Thr17 residues. Phosphorylation of the Thr17 residue requires both stimulation of the CaMKII signaling pathways and inhibition of PP1, the major phosphatase that dephosphorylates PLN. These two prerequisites appear to be fulfilled by ß-adrenoceptor stimulation, which as a result of PKA activation, triggers the activation of CaMKII by increasing intracellular Ca2+, and inhibits PP1. Several pathological situations such as ischemia-reperfusion injury or hypercapnic acidosis provide the required conditions for the phosphorylation of the Thr17 residue of PLN, independently of the increase in PKA activity, i.e., increased intracellular Ca2+ and acidosis-induced phosphatase inhibition. Our results indicated that PLN was phosphorylated at Thr17 at the onset of reflow and immediately after hypercapnia was established, and that this phosphorylation contributes to the mechanical recovery after both the ischemic and acidic insults. Studies on transgenic mice with Thr17 mutated to Ala (PLN-T17A) are consistent with these results. Thus, phosphorylation of the Thr17 residue of PLN probably participates in a protective mechanism that favors Ca2+ handling and limits intracellular Ca2+ overload in pathological situations.
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Biliary atresia (BA) is classically described at the neonatal age. However, rare cases of BA in older infants have also been reported. We report four cases of late-onset BA in infants older than 4 weeks (3 males, 1 female), and describe the diagnostic and management difficulties. One of the cases had a late-onset (29 weeks) presentation with a successful surgical procedure. We highlight the importance of this unusual differential diagnosis in infants with cholestatic syndrome, who may benefit from Kasai surgery, regardless of age.
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INTRODUCTION: C4d is a marker of antibody-mediated rejection (ABMR) in kidney allografts, although cellular rejection also have C4d deposits. OBJECTIVE: To correlate C4d expression with clinico-pathological parameters and graft outcomes at three years. METHODS: One hundred forty six renal transplantation recipients with graft biopsies by indication were included. C4d staining was performed by paraffin-immunohistochemistry. Graft function and survival were measured, and predictive variables of the outcome were determined by multivariate Cox regression. RESULTS: C4d staining was detected in 48 (31%) biopsies, of which 23 (14.7%) had diffuse and 25 (16%) focal distribution. Pre-transplantation panel reactive antibodies (%PRA) class I and II were significantly higher in C4d positive patients as compared to those C4d negative. Both glomerulitis and pericapillaritis were associated to C4d (p = 0.002 and p < 0.001, respectively). The presence of C4d in biopsies diagnosed as no rejection (NR), acute cellular rejection (ACR) or interstitial fibrosis/ tubular atrophy (IF/TA) did not impact graft function or survival. Compared to NR, ACR and IF/TA C4d-, patients with ABMR C4d+ had the worst graft survival over 3 years (p = 0.034), but there was no difference between ABMR versus NR, ACR and IF/TA that were C4d positive (p = 0.10). In Cox regression, graft function at biopsy and high %PRA levels were predictors of graft loss. CONCLUSIONS: This study confirmed that C4d staining in kidney graft biopsies is a clinically useful marker of ABMR, with well defined clinical and pathological correlations. The impact of C4d deposition in other histologic diagnoses deserves further investigation.
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There are complex and diverse methodological problems involved in the clinical and epidemiological study of respiratory diseases and their etiological factors. The association of urban growth, industrialization and environmental deterioration with respiratory diseases makes it necessary to pay more attention to this research area with a multidisciplinary approach. Appropriate study designs and statistical techniques to analyze and improve our understanding of the pathological events and their causes must be implemented to reduce the growing morbidity and mortality through better preventive actions and health programs. The objective of the article is to review the most common methodological problems in this research area and to present the most available statistical tools used.
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OBJECTIVE: To assess overall survival of women with cervical cancer and describe prognostic factors associated. METHODS: A total of 3,341 cases of invasive cervical cancer diagnosed at the Brazilian Cancer Institute, Rio de Janeiro, southeastern Brazil, between 1999 and 2004 were selected. Clinical and pathological characteristics and follow-up data were collected. There were performed a survival analysis using Kaplan-Meier curves and a multivariate analysis through Cox model. RESULTS: Of all cases analyzed, 68.3% had locally advanced disease at the time of diagnosis. The 5-year overall survival was 48%. After multivariate analysis, tumor staging at diagnosis was the single variable significantly associated with prognosis (p<0.001). There was seen a dose-response relationship between mortality and clinical staging, ranging from 27.8 to 749.6 per 1,000 cases-year in women stage I and IV, respectively. CONCLUSIONS: The study showed that early detection through prevention programs is crucial to increase cervical cancer survival.
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Male mice (NMRI strain) of 3 and 5 g were inoculated i. p. with 8 x 10(6) and 9 x 10(4) metatrypomastigotes/g harvested from a 12-day-old LIT culture of Trypanosoma rangeli of the "Dog-82" strain. At regular intervals after inoculation, the animals were sacrificed and portions of heart, liver, spleen, lung, thigh, kidney, stomach, intestine, brain, sternum, and vertebral column were embedded in paraffin, sectioned, and stained with haematoxylin-eosin and Giemsa colophonium. Pathology was encountered in the first five tissues cited above. The subcutaneous, periosteal, interstitial, and peribronchial connective tissues, and later the muscle cells of the heart, were heavily parasitized by amastigotes and trypomastigotes. The possible reasons for the decrease in tissue parasitosis at the same time that the parasitemia is reaching its peak, and for the low level of inflammation in the parasitized tissues, are discussed. The observations of other workers, as well as the results described here, indicate that certain strains of T. rangeli under certain conditions may well cause pathological alterations in mammals.