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Background: In endemic areas, visceral leishmaniasis has been identified as an opportunistic infection in patients with derangements in their cellular immune system., Methods: We report a renal transplant patient with visceral leishmaniasis. We also reviewed the previously published cases of 17 organ transplant recipients with this parasitic disease., Results: Visceral leishmaniasis occurred a median time of 8 months after transplantation, and the clinical picture was characterized by fever, splenomegaly, and blood cytopenias. Leishmaniae were detected in bone marrow in 16 of 18 patients and diagnostic serology results were found in 8 of 10 tested patients. Pentavalent antimonials were used to treat 16 patients, five of which developed pancreatitis. Five of 18 patients died, including two untreated patients. Relapses of visceral leishmaniasis occurred in 4 of 13 survivors., Conclusions: In endemic areas, visceral leishmaniasis may complicate the clinical course of organ transplantation and can have fatal consequences, particularly when untreated.

Trichomonas vaginalis possesses a membrane-associated neuraminidase activity that is released into culture medium during its growth in vitro. The neuraminidase shows an optimum pH of 4.5 and a Km of 0.15 mM for 2'-(4-methylumbelliferyl)-alpha-D-N-acetyl-neuraminic acid as a substrate. This enzyme releases mainly alpha-2,3-linked sialic acid because it is able to liberate sialic acid from sialyllactose (mainly alpha-2,3) but not from mucin (alpha-2,6) or fixed erythrocytes (mainly alpha-2,6). The neuraminidase activity is strongly inhibited by 2,3-dehydro-2-deoxy-N-acetyl neuraminic acid, whereas EGTA and Ca2+ do not affect the activity. Gel filtration-fast protein liquid chromatography of culture supernatant displays a single peak of neuraminidase activity with molecular weight 52,000. The levels of neuraminidase activity are variable in fresh and long-term grown isolates of T. vaginalis, regardless of time in culture. However, there are 2 kinds of isolates, 1 group with high neuraminidase activity and able to secrete the enzyme during growth and the other with low neuraminidase activity. The results suggest that T. vaginalis possesses a membrane-associated neuraminidase that is present to a variable degree in different isolates.

PEHPS medium, developed for axenic cultivation of Entamoeba histolytica and E. invadens, was also capable of supporting the growth of a Trichomonas vaginalis strain, with an inoculum of 1 to 100 trichomonads/ml. The logarithmic growth phase in PEHPS or in TYI-S-33 medium lasted 72 h; yield (3.33 +/- 0.56 x 10(6) trichomonads/ml), duplication time (4.27 h), number of duplications (16.85), or increase ratio (33,328) in PEHPS medium showed no significant differences with those obtained in TYI-S-33 under similar culture conditions. Accordingly, PEHPS medium might be used for the axenic cultivation of T. vaginalis.

Methods: Five patients with a family history of hypercholesterolemia were treated for one year with double filtered technique of LDL-apheresis: heterozygotic in four patient and homozygotic in one. All patients presented documented cardiovascular disease and had been treated unsuccessfully with lipid lowering drugs., Results: Plasmatic cholesterol was significantly reduced from 463.8 +/- 60.9 mg/dl to 326.36 +/- 36 mg/dl at 6 months after treatment and 347.56 +/- 68.1 mg/dl at 12 months (p < 0.05). LDL was also reduced from 407.92 +/- 69.39 mg/dl to 294.04 +/- 62.02 mg/dl and 296.6 +/- 82.42 mg/dl respectively (p < 0.05) and Apo B was reduced from 291.84 +/- 28.97 mg/dl to 224.5 +/- 47.11 mg/dl at 6 and 12 months respectively, without significant modifications of other lipidic parameters and without adverse events., Conclusions: LDL-apheresis is a therapeutic approach effective in the reduction of total plasmatic cholesterol, in conjunction with to LDL and APO B in patients refractory to lipid lowering agents.

During the 1992 and 1993 field seasons, several new specimens of Branisella boliviana, the oldest fossil platyrrhine, were discovered in the late Oligocene deposits at Salla, northwestern Bolivia. The new materials are two maxillary fragments and seven mandibular fragments, including P3 and P2, neither of which have previously been recovered. All new and previously reported materials, including the holotype and referred specimens, were apparently recovered from the same horizon, called the Branisella zone (MacFadden et al. [1985] J. Geol. 93:223-250; MacFadden [1990] J. Hum. Evol. 19:7-21. The crown morphology of the newly discovered upper and lower premolars suggests that Branisella has a close affinity with callitrichines. A detailed examination of all molar specimens suggests that "Szalatavus attricuspis," which was recovered at Salla in 1981 and described as a new genus by Rosenberger et al. (1991), is a junior synonym of Branisella. The Branisella-like upper molar, in which a small hypocone is preserved on the poorly developed distolingual cingulum, is a shared-derived character with callitrichines and does not correspond to the primitive state for platyrrhine phylogeny. The ancestral upper molar morphotype for platyrrhines should have a moderate to large hypocone and a well developed talon area.

The in vitro cytopathic effect of Trichomonas vaginalis on epithelial cells was explored through the interaction of trophozoites of the virulent strain GT-10 with MDCK monolayers. The interaction was analyzed through electrophysiology, video microscopy, and transmission and scanning electron microscopy. Electrical measurements revealed that living parasites produced severe damage to the cell monolayers within 30 min, manifested as a rapid decrease in transepithelial resistance. Microscopic observations demonstrated that when placed in contact with epithelial cells, trichomonas formed clumps through interdigitations and transient plasma membrane junctions between adjacent parasites. Also, attached trophozoites adopted an ameboid shape. The in vitro cytopathic action of T. vaginalis on MDCK cells was initially evident by modifications of the plasma membrane, resulting in opening of tight junctions, membrane blebbing, and monolayer disruption. After 15 min of interaction the damage was focal, concentrating at sites where parasite clumps adhered to the monolayer. At 30 min practically all MDCK cells were dead, whether or not trichomonas were attached to them. These events were followed by detachment of lysed cells and complete disruption of the monolayer at 60 min. Electron microscopy demonstrated a peculiar form of adhesion that appears to be specific for trichomonas, in which the basal surface of T. vaginalis formed slender channels through which microvilli and cytoplasmic fragments of epithelial cells were internalized. The same sequence of lytic events was found with the less virulent GT-3 strain. However, the time course of cytolysis with GT-3 parasites was much slower, and lysis was limited to areas of attachment of T. vaginalis.

The objective of this investigation was to quantitatively evaluate, by using light and transmission electron microscopy, the intracellular digestion of human erythrocytes (HE), ingested by Entamoeba histolytica trophozoites in vitro. Amebas fed 10 min with HE were postincubated 3-12 h at 36.5 degrees C without HE, and fixed with glutaraldehyde. After staining by the benzidine reaction, HE per ameba, and percent of amebas containing at least one HE were determined by light microscopy. Trophozoites ingested an average of eight HE per ameba and 92% of them contained HE after the 10 min pulse. Erythrocytes were clearly observed as reddish-brown corpuscles in the amebic cytoplasm. During postphagocytosis incubations progressive loss of HE staining, as well as changes in size of food vacuoles, were observed, thus proving the intracellular digestion of HE. The hydrolysis of HE was corroborated with the electron microscope, the HE cytoplasmic matrix being the first structure catabolized and later the plasma membrane. Quantitative analysis demonstrated decrease of 56% of ameba containing HE, and 1.35 HE per ameba on average, after 3 h postphagocytosis. Afterwards, both parameters decreased at a slow rate until HE disappeared. The t1/2 of HE within amebas was 2 h.

The effect on amebal virulence of Escherichia coli, Clostridium symbiosum and a mixture of lactobacilli was investigated. Amebas from HM1 and HK axenic strains were incubated with a single bacterial strain or lactobacilli for short, intermediate, or long periods and analyzed for their erythrophagocytosis, hemolytic activity and cytotoxicity in vitro and hepatic abscesses formation in vivo. It was found that in vitro virulence was enhanced by all studied bacteria in HK9 but not in HM1 strains, which only showed an increase in cytotoxicity. The virulence in vivo was solely increased in trophozoites of HM1 strain by all tested bacteria.

A simplified and reliable method to quantify Entamoeba histolytica cytotoxicity was standardized. Mice spleen leucocytes were utilized as target cells. Interaction time was reduced to 1 h by pelleting interacting cells. To assess target-cell killing by amoebae, a nigrosine exclusion test was employed. Fixation with glutaraldehyde stabilized the percentage of stained target cells. Similar results were obtained when cytotoxicity of the E. histolytica HM1 strain was tested by the traditional and proposed methods. The new method allowed quantification of the contribution of cytolysis and cytophagocytosis to amoebic cytotoxicity. It was also demonstrated that uncloned E. histolytica HM1 strain is a heterogeneous population with respect to cytotoxicity expression.

8 cases of membranous glomerulonephritis (MG) after renal transplants (RT) are presented; one being a recurrence of the original disease and the other 7 due to a different cause of renal insufficiency. The total incidence of MG after transplantation was 1.63%; 1.39% being the incidence of MG of new cases. Only 1 patient showed decrease of renal function and in this case the MG was accompanied by chronic rejection lesions. There was no sign of neoplasias nor drugs producing MG. As far as chronic infections are concerned, only one patient showed B antigen and it was not observed during the immunofluorescent test in the biopsy. 6 patients had urological complications after the renal transplant (3 cases of urinary fistula; 2 cases of obstructive uropathy; 1 case of short ureter). 2 patients experienced the start of hemodialysis due to focal and segmentary glomerulosclerosis. The beginning of proteinuria commences between 2 and 23 months after the RT (median 13,0 +/- 7,5 moths); with a range of between 2.0 and 12.0 gr/day (median: 6.8 +/- 3,2 Z gr/day), this being nephrotic in 4 cases. Proteinuria improved 1 case, and persisted in the other patients at the same level registered previous to the diagnosis. MG is a non-frequent complication or RT and is usually benign. Patients with post-transplant urologic complications could be considered to have a higher risk of developing a MG "de novo".

From 1974 to 1987 we have diagnosed thirty three patients with rheumatic fever. The age of onset ranged from three to sixteen years with a mean age of nine years and six months. Carditis was the most frequent major criteria (27/33) followed by arthritis (14/33) and Sydenham's chorea (6/33). All the patients with carditis had the mitral valve affected. The usual treatment in the acute phase was penicillin and aspirin. The prophylaxis recommended to the patients was penicillin G benzatine every 21 days if they had carditis and every 28 days if they didn't. Two patients allergic to penicillin are receiving erythromycin. We have observed that the incidence of rheumatic fever has remained unchanged that the age of onset increased and that the antiinflammatory drug of choice in most patients with carditis is aspirin.

The effectiveness of antibiotic prophylaxis was evaluated in the immediate postoperative period of renal transplantation (RT). Before RT, the patients were randomly assigned to one of the following groups: 1) cefotaxime (intravenous infusion of 1 g one hour before the operation). 2) Ceftriaxone (1 g i.v. given in a similar way). 3) Control (without antibiotics). Patients who required antibiotic therapy during the first 3 postoperative weeks were excluded. 20 recipients of cadaveric renal grafts were included in each group. There were 39 males and 21 females with a mean age of 39.9 years. One patient from the cefotaxime group (5%), 2 from the ceftriaxone group (10%) and 2 from the control group (10%) developed infection of the surgical wound, all due to grampositive organisms. 19 patients had urinary tract infections: 7 from the control group (35%), 7 from the cefotaxime group (35%), and 5 from the ceftriaxone group (25%). The development of wound infection was not correlated with urea, creatinine, hemoglobin or total protein levels, or with urinary tract infection or fistula, diabetes or fever. The mean packed red cell volume of the patients who developed wound infection was 24.7 +/- 1.2 vs 28.6 +/- 6.6 in those who did not (p less than 0.01). All patients with visible hematoma and 3 of 10 with perirenal blood collection had wound infection. It was concluded that antibiotic prophylaxis for renal transplantation was useless in our patients.

Some strains of mice are known to be relatively resistant to hepatic or intestinal amebic infections. In order to know if the intestinal resistance is expressed few hours after infection, we inoculated axenic amebae in three inbred strains of mice either by direct intracecal injection or by infection of a washed-closed cecal loop. We found that amebae do not survive in conventional animals but they colonize longer in animals with the cecal loop. However, the survival was low after 24 hours postinfection. Balb/c mice were more susceptible and CBA mice more resistant. Our results suggest that genetic resistance to intestinal amebiasis is expressed in mice in the early phases of infection.

A morphological analysis of an experimental model of invasive intestinal amebiasis was carried out using the washed-closed cecal loop model in hamsters and guinea-pigs. By light microscopy, few amebic trophozoites adhered to the intestinal epithelium, whereas many associated to the mucus blanket. Some trophozoites attached to the interglandular epithelium, during the first 10 to 15 hours of interaction. Hereafter, the parasites destroyed gradually the epithelium and were associated with normal and lysed inflammatory cells. Some amebas have cell debris and erythrocytes in their cytoplasms. Typical amebic ulcer contained abundant trophozoites at the basolateral area. The results suggest that intestinal mucus and muscularis mucosa are temporal barriers to amebic invasion and extension of the ulcer. At the mucosal and submucosal levels, lysis of inflammatory cells produced by amebas seems to play an important role in the extension of the ulcer.

The results of five 'en bloc' kidney transplants from 5 anencephalic newborns are reported. The receptors were 8-50 years old. The graft survival 12 months after transplantation was 60%. The average plasma creatinine level the 1st month after transplantation was 4.0 +/- 0.8 mg/dl, after 6 months 1.5 +/- 0.8, and is currently 1.2 +/- 0.6 mg/dl. The follow-up time ranged from 17 to 55 months (mean 30.3 +/- 17.5 months). Two grafts were lost during the early posttransplantation period (due to arterial thrombosis and vascular rejection, respectively); the other grafts are still functioning. Two grafts showed initial oliguria. All of the patients required hemodialysis or peritoneal dialysis for 5-60 days (mean 22.5 +/- 21.4 days). The time of cold ischemia ranged from 15 to 35 h (mean 25.6 +/- 7.7 h). The literature published on the subject is reviewed, and it is concluded that anencephalic donors are an acceptable option for transplantation.

The complete sequence of morphologic events during amebic liver abscess formation in the hamster has been studied, from the lodgement of amebas in the hepatic sinusoids to the development of extensive liver necrosis. Following intraportal inoculation of live amebas, the early stages of the lesion (from 1 to 12 hours) were characterized by acute cellular infiltration composed of an increasingly large number of polymorphonuclear leukocytes, which surrounded centrally located trophozoites. Histiocytes and lysed leukocytes were situated on the periphery of the lesions. Hepatocytes close to the early lesions showed degenerative changes which led to necrosis; however, direct contact of liver cells with amebas was very rarely observed. At later stages, the extent of necrosis increased, macrophages and epithelioid cells replaced most leukocytes, and well-organized granulomas developed. Extensive necrosis associated with fused granulomas was present by Day 7. The results suggest that Entamoeba histolytica trophozoites do not produce amebic liver abscesses in hamsters through direct lysis of hepatocytes. Rather, tissue destruction is the result of the accumulation and subsequent lysis of leukocytes and macrophages surrounding the amebas.

Cell-mediated immunity in vivo was studied by delayed cutaneous hypersensitivity (DCH) to seven antigens in 156 chronic haemodialysis (HD) patients, using a disposable multipuncture device. Anergy was found in 46.8 per cent of patients, and a positive correlation was seen between anergy and female sex, time on HD, glomerulonephritis as primary renal disease, younger age and previous blood transfusions (BT). The effect of BT on DCH was studied prospectively in 29 responsive patients. A significant decrease in DCH response was seen. The transfusion-induced anergy remained for a variable time. The pretransplant BT policy suggested by our data would be to periodically undertake skin tests and to transfuse only responsive patients, thereby avoiding the adverse effects of multiple BT.

To determine the incidence of renal involvement in Schönlein-Henoch syndrome, authors enrolled in a prospective study all children admitted with this diagnoses from 1971 through 1978. They followed-up 112 patients, which represented the 2 per one thousand of the total hospital pediatric admission in the same period; 22 patients (19.6%) developed renal involvement. After two years of follow-up they observe one patient with progressive renal failure, four with minor urinary abnormalities and 17 asymptomatics. The single patient with renal failure represents the 4.5% of the patients with Schönlein-Henoch nephropathy and the 0.9% of the total affected with this syndrome.

A new experimental model for the production of early stages of invasive intestinal amebiasis in hamsters or guinea pigs with axenic or monoxenic cultures of Entamoeba histolytica of the HM1:IMSS strain is reported. The model is called the washed-closed cecal loop, because it involves the washing out of the cecum contents of conventionally raised animals and the formation of a closed loop, into which amebas are inoculated. Colonization occurred in all inoculated animals. After 48 hr, macroscopic ulcerations of the cecal mucosa were found in approximately one-half (5/12) of the animals inoculated with axenic amebas and in more than two-thirds (10/12) of those inoculated with monoxenic parasites. The amebic nature of the mucosal ulcerations was confirmed by light and transmission electron microscopy, as well as by scanning electron microscopy (SEM) of fractured samples of cecal mucosa. SEM provided a rapid and reliable technique to assess both the extent and the nature of the lesions. This model is particularly useful for the study of the pathogenesis of early intestinal lesions produced by virulent amebas, and may also be applied to experimental studies on the immunology of invasive intestinal amebiasis.

The morphological features of early intestinal ulcerations induced in rodents with axenic cultures of Entamoeba histolytica were studied by scanning and transmission electron microscopy. Amebas did not attach to the luminal surface of the mucosa except at interglandular regions, where parasites penetrated apparently through pseudopodial movement. Once in the lamina propria, trophozoites multiplied and destroyed mucosal components. Damage extended laterally through the mucosa, but progression to deeper layers of the intestinal wall was prevented by the muscularis mucosae, which acted as a partial barrier. This was eventually breached at focal points where amebas invaded the submucosa. Electron microscopy clearly showed the lysis of abundant polymorphonuclear neutrophil leukocytes (PMNs) by the amebas at the periphery of intestinal ulcerations as well as the lack of bacteria at these sites. This study demonstrates that recruitment and destruction of inflammatory cells following intestinal amebic invasion may take place in the absence of bacterial multiplication. The observations provide histological support to the hypothesis that lysis of PMNs by trophozoites participates in the genesis of amebic intestinal lesions.

The in vitro activity of the antibacterial agent nalidixic acid (HNal) and its iron (III) complex (FeNal) against Entamoeba histolytica HM1 strain trophozoites in axenic or monoxenic (associated with Clostridium symbiosum) cultures was investigated. Using a dilution test with TYI-S-33 medium, this protozoan was found to be susceptible to both drugs, but FeNal showed amoebicidal activity only at concentrations higher than those used with HNal.