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Only one study previously mentioned the involvement of colon during Taenia taeniaeformis larvae infection in rats with inconsistent occurrence of lesions. Present study aimed to determine the consistency of histopathologic changes in colonic epithelia, and the proliferation of mucosal cells through BrdU and PCNA immunohistochemistry. Results demonstrated that crypt hyperplasia of the colon was found in all infected rats, although variable in degree even in a single tissue section. Cystic cavities were frequently seen in severely hyperplastic mucosa. Proliferative zone lengths were significantly increased and PCNA positive cells were observed throughout the colonic crypt lengths at 9 but not at 6 weeks post infection. Cell proliferation involving the major types of cells in the epithelial colon was also increased in infected rats at 9 weeks post infection, with labeling indices significantly greater than the control rats throughout the BrdU time course labeling. Findings suggested that massive increases in epithelial cells and depth of colonic crypts were due to a remarkable increase in cell proliferation. The study concluded that enteropathy in the colon during T. taeniaeformis infection could be consistently observed in heavily infected rats.

In this study, we verified the possible role of cyclophosphamide (CY) in protecting or not against neuronal losses in young and aged male Calomys callosus chronically infected with the MORC-1 strain of Trypanosoma cruzi through numerical quantification of neurons from the myenteric plexus of the colon and quantification of nitric-oxide concentration (NO) during the acute and chronic phase of infection. For this purpose, groups of young C. callosus were infected with the MORC-1 strain of T. cruzi. A group of infected animals received i.p. 0.2 mg/ml genuxal dissolved in distilled water treatment with CY. NO concentration in aged animals displayed reduced levels when compared to those found in young animals. No significant alterations in the number of neurons were observed in young animals, but for aged ones, a protective role of CY in reducing neuron loss was noted, in addition to enhancing the neuronal volume, area, and perimeter. These results suggest that CY administration, depending on the dose and time span, can act as a protective agent against neuronal losses.

Aim: The application of ultrasound may be suitable for evaluating the effects of intestinal cytoskeletal rearrangement of the duodenum and colon as a result of exposure to live Giardia lamblia trophozoites. We studied the sonographic appearance of the duodenum and colon in giardiasis compared with amebiasis and healthy subjects., Methods: Sonographic images obtained from 100 consecutive patients with symptomatic giardiasis were compared to those taken from 40 patients with amebiasis and 40 healthy subjects. B-mode ultrasound examination of the duodenum and colon was performed using a 7.5 MHz annular array transducer. Gray scale images with water contrast were acquired., Results: Normal duodenum and colon echoanatomy were demonstrated. Giardial lesions of the duodenum and colon were associated with increased wall thickness when compared with healthy subjects (P < 0.05). Furthermore, giardial lesions were characterized by increased wall echogenicity, flattening or loss of duodenal folds and/or colonic haustration, hyperechoic floating foci (HFF) demonstrating chaotic motility, increased peri-lesional tissue echogenicity, and altered colonic peristalsis. In amebiasis, focal hyperechoic wall thickening was seen at lesion sites identified as amebomas with increased wall echogenicity, but otherwise normal duodenal folds and colonic haustration. There were no HFF with chaotic motility, rather intestinal contents showed bulk motility in patients with amebiasis. There was no focal colonic wall motion abnormality observed., Conclusion: B-mode imaging with water contrast demonstrated details of duodenal and colonic echoanatomy. There were sonographic features of giardial lesions of the duodenum and colon that were distinct from those in amebiasis and healthy subjects.

Intestinal lymphoid tissues and Peyer's patches (PP) are innervated sites of immune surveillance in the gastrointestinal tract. Following infection with F. hepatica, neuronal hyperplasia and significantly increased eosinophil and mast cell trafficking to colonic PP sites were evident in rat tissues. Nerve-eosinophil associations were significantly elevated in infected colon and colonic PP, as were colonic tissue levels of the circulatory recruitment factors IL-5 and eotaxin. Increased immunoreactivity for neuronal plasticity markers GAP-43 and neural cell adhesion molecule (NCAM) was also found in infected tissues. Such neuronal alterations in the PP during enteric parasitism may have functional consequences on particular or pathogen uptake.

A female boa (Boa constrictor) from a zoological collection was submitted for necropsy after sudden death. Prominent pathological findings included a diphtheroid colitis, endoparasitism, focal pneumonia and inclusion bodies typical for inclusion body disease (IBD). In the colon entamoebae were identified, which differed in size and distribution from Entamoeba invadens. Gene sequence analysis of the 18S ribosomal RNA revealed 100% similarity with an Entamoeba species from the African bullfrog (Pyxicephalus adspersus), probably Entamoeba ranarum. The snake was possibly immunosuppressed, and the source of infection remains unclear. This is the first report of an infection with an amphibian Entamoeba species associated with colitis in a snake.

Blastocystis is a ubiquitous enteric protozoan found in the intestinal tracts of humans and a wide range of animals. Evidence accumulated over the last decade suggests association of Blastocystis with gastrointestinal disorders involving diarrhea, abdominal pain, constipation, nausea, and fatigue. Clinical and experimental studies have associated Blastocystis with intestinal inflammation, and it has been shown that Blastocystis has potential to modulate the host immune response. Blastocystis is also reported to be an opportunistic pathogen in immunosuppressed patients, especially those suffering from AIDS. However, nothing is known about the parasitic virulence factors and early events following host-parasite interactions. In the present study, we investigated the molecular mechanism by which Blastocystis activates interleukin-8 (IL-8) gene expression in human colonic epithelial T84 cells. We demonstrate for the first time that cysteine proteases of Blastocystis ratti WR1, a zoonotic isolate, can activate IL-8 gene expression in human colonic epithelial cells. Furthermore, we show that NF-kappaB activation is involved in the production of IL-8. In addition, our findings show that treatment with the antiprotozoal drug metronidazole can avert IL-8 production induced by B. ratti WR1. We also show for the first time that the central vacuole of Blastocystis may function as a reservoir for cysteine proteases. Our findings will contribute to an understanding of the pathobiology of a poorly studied parasite whose public health importance is increasingly recognized.

Treatment of higher eukaryotic cells with short-chain fatty acids (SCFA) such as butyrate causes decreased levels of histone deacetylase (HDAC) activity and hyperacetylation of histones, and thereby affects gene expression, cell growth and differentiation. Entamoeba parasites encounter high levels of SCFA in the host colon, and in vitro these compounds allow trophozoite stage parasites to multiply but prevent their differentiation into infectious cysts. The Entamoeba invadens IP-1 histone H4 protein has an unusual number of lysines in its N-terminus, and these become hyperacetylated in trophozoites exposed to the HDAC inhibitors trichostatin A (TSA) or HC-toxin, but not in trophozoites exposed to butyrate. We have now found that several other commonly studied isolates of Entamoeba parasites also have an extended set of histone H4 acetylation sites that become hyperacetylated in response to TSA, but hypoacetylated in response to butyrate, suggesting an unusual sensitivity of this parasite's histone modifying enzymes to SCFA. Butyrate was found to enter trophozoites in a pH-dependent manner consistent with diffusive entry of the un-ionised form of the fatty acid into the amoebae. Transit of the Entamoeba organism through areas of the host intestine with distinct pH and SCFA concentrations would therefore result in very different levels of SCFA within the parasite. Entamoeba appears to have acquired unique alterations of its histone acetylation mechanism that may allow for its growth in the presence of varying amounts of the bacterial fermentation products.

Recent World Health Organization (WHO) reports estimate that 500-600 million people worldwide are at risk of schistosomiasis. In areas of high prevalence of hepatitis C (HCV) and schistosomiasis there is an increased risk for end-stage liver disease. Liver transplant is a viable option for those with HCV or other liver pathology and schistosomiasis. Posttransplant recurrence of schistosomiasis has rarely been described. We report a case of posttransplant recurrence of schistosomiasis.

Ciliates of the subclass Trichostomatia inhabit the fermentative regions of the digestive tract of herbivores. Most available small subunit ribosomal RNA (SSrRNA) gene sequences of trichostomes are from species isolated from the rumen of cattle or sheep and from marsupials. No ciliate species endosymbiotic in horses has yet been analyzed. We have sequenced the SSrRNA genes of five ciliate species, isolated from the cecum and colon of four Yakut horses: Cycloposthium edentatum, Cycloposthium ishikawai, Tripalmaria dogieli, Cochliatoxum periachtum, and Paraisotricha colpoidea. Based on their morphology, Cycloposthium, Tripalmaria, and Cochliatoxum are classified as Entodiniomorphida, while Paraisotricha is considered a member of the Vestibuliferida. Phylogenetic analyses using Bayesian inference, distance, and parsimony methods confirm these placements. The two Cycloposthium species cluster together with the published Cycloposthium species isolated from a wallaby in Australia. Tripalmaria and Cochliatoxum branch as a sister group to or basal within the Entodiniomorphida. The Vestibuliferida remain paraphyletic with Paraisotricha and Balantidium branching basal to all other trichostome species, but not closely related to Isotricha and Dasytricha.

Objective: To investigate the effects of intraperitoneal injected schistosome ova on TNBS-induced colitis and on the intestinal TLR4 expression in mice., Methods: 40 BALB/c mice were randomized into 3 groups: normal control group (10 mice), TNBS group (20 mice) in which mice were exposed to trinitrobenzesulfonic acid (TNBS) and were induced with colitis, and the schistosome ova group (10 mice) in which mice were intraperitoneal injected with freeze-killed schistosome ova and later exposed to TNBS. The following variables were observed: mortality, pathological appearance of the colon, histological scoring of the specimen, serum TNF-alpha level, and intestinal TLR4 expression detected by RT-PCR and Immunohistochemistry., Results: Mortality of schistosome ova group was lower than that of the TNBS group (20% vs 70%, P < 0.05). Inflammation of the mice colon in the schistosome ova group was less severe than that of the TNBS group (1.4 +/- 0.5 vs 4.2 +/- 0.6, P < 0.01, Ameho criteria scoring). TLR4 expression of colon was up-regulated in mice of TNBS group and down-regulated in schistosome ova group which was still higher than that of normal controls (0.762 +/- 0.054 vs 0.325 +/- 0.029 vs 0.237 +/- 0.021, P < 0.01)., Conclusion: Intraperitoneal injected schistosome ova can obviously reduce TNBS-induced colitis in mice, which may be attributed to down-regulated TLR4 expression in colon.

Cysteine proteinases are key virulence factors of the protozoan parasite Entamoeba histolytica. We have shown that cysteine proteinases play a central role in tissue invasion and disruption of host defenses by digesting components of the extracellular matrix, immunoglobulins, complement, and cytokines. Analysis of the E. histolytica genome project has revealed more than 40 genes encoding cysteine proteinases. We have focused on E. histolytica cysteine proteinase 1 (EhCP1) because it is one of two cysteine proteinases unique to invasive E. histolytica and is highly expressed and released. Recombinant EhCP1 was expressed in Escherichia coli and refolded to an active enzyme with a pH optimum of 6.0. We used positional-scanning synthetic tetrapeptide combinatorial libraries to map the specificity of the P1 to P4 subsites of the active site cleft. Arginine was strongly preferred at P2, an unusual specificity among clan CA proteinases. A new vinyl sulfone inhibitor, WRR483, was synthesized based on this specificity to target EhCP1. Recombinant EhCP1 cleaved key components of the host immune system, C3, immunoglobulin G, and pro-interleukin-18, in a time- and dose-dependent manner. EhCP1 localized to large cytoplasmic vesicles, distinct from the sites of other proteinases. To gain insight into the role of secreted cysteine proteinases in amebic invasion, we tested the effect of the vinyl sulfone cysteine proteinase inhibitors K11777 and WRR483 on invasion of human colonic xenografts. The resultant dramatic inhibition of invasion by both inhibitors in this human colonic model of amebiasis strongly suggests a significant role of secreted amebic proteinases, such as EhCP1, in the pathogenesis of amebiasis.

In cases of fulminant amoebic colitis we have determined the interactions between Entamoeba histolytica trophozoites and immune cells in order to better understand the pathophysiology of amoebic colitis. Eleven specimens of amoebic colitis and five specimens of colon without amoebic lesions were studied. Trophozoites and immune cells were located by topographic stains, histochemistry and immunohistochemistry. Trophozoites were seen in both damaged and undamaged areas of the colonic mucosa. Specimens of fulminant amoebic colitis showed: (a) an increase in IgA+, IgG+ B cells and neutrophils; (b) a reduction in IgM+ B cells, CD8+ T cells, macrophages, eosinophils and mast cells; and (c) no change in the number of NK and CD4+ T cells. The cellular infiltrate in amoebic colitis may represent the combined effects of amoebic monocyte locomotion inhibitory factor and switching of IgM+ B cells to IgG+ and IgA+ plasma cells, induced by amoebic antigens. Tissue damage in the absence of trophozoites may result from ischaemia or host immune responses.

Most humans infected with the virulent protozoan parasite Entamoeba histolytica do not develop invasive disease. Available evidence indicates that beneficial bacteria and the mucus gel layer in the colon lumen protect the host mucosa. Glycosidases produced by some normal colonic bacteria and luminal proteases degrade the key adherence lectin on E. histolytica trophozoites and decrease their adherence to epithelial cells. The mucus gel layer prevents those trophozoites that escape the hydrolases from reaching the epithelial cells. Trophozoite mucosal invasion is triggered only when both protective mechanisms are lost, as might occur during an unrelated pathogenic enteric bacterial infection. A newly developed gnotobiotic model of intestinal amebiasis should enable testing of this hypothesis and provide clues to help design practical studies in humans.

We describe a case of Cryptosporidium infection occurring in a child after allogeneic SCT for acute non-lymphoblastic leukemia. This patient presented an intestinal, biliar, and pancreatic Cryptosporidium disease associated with an intestinal aGvHD. The increase in CD3+/CD4+ cells secondary to the reduction of steroid therapy associated with the improvement of aGvHD and the use of antiparasitic treatments (especially nitazoxanide) improved the infection-related symptoms and led to a complete clearance of the Cryptosporidium.

Lactating rats experience a breakdown of immunity to parasites, i.e. they carry larger worm burdens after re-infection compared to their non-lactating counterparts. Feeding high-protein foods to lactating rats results in reduced worm burdens. This could be attributed to changes in gastrointestinal environment or to overcoming effects of nutrient scarcity on host immunity. The latter hypothesis was addressed through a manipulation of nutrient demand by manipulating litter size. Twenty-three rats were immunized prior to mating and re-infected on day 2 of lactation with 1600 infective Nippostrongylus brasiliensis larvae. From parturition onwards, rats received ad libitum low-protein food (100 g crude protein/kg). Litter size were standardised to nine (LS9), six (LS6) or three (LS3) pups, by day 2 of lactation. After a further 10 d, LS9 and LS6 rats carried more worms than LS3 rats. However, feeding treatment did not affect concentrations of mucosal inflammatory cells. Achieved feed intake did not differ consistently between the treatment groups. However, LS9 and LS6 rats lost weight, whilst LS3 rats gained weight during lactation. The results support the view that resistance to N. brasiliensis is sensitive to changes in nutrient demand, and the improved resistance to N. brasiliensis is likely due to effects of overcoming nutrient scarcity on host immunity.

The work aimed to study the effect of Schistosoma mansoni (S. mansoni) on gastrointestinal transit and contractility of the colonic muscles of two subgroups of experimental mice, infected by 50 & 200 cercaria/mouse respevtively, at 8th & 12th week postinfection (PI). In addition, the histopathologic changes in the colon, and the immunological changes of the host were studied at different durations. At 8th weeks PI, in both subgroups, gastrointestinal transit was statistically significant decreased, in concurrent with statistically significant increase in the colonic muscle contractility compared to the controls. The colon was inflamed as shown by mucosal inflammatory infiltrates, with large size and number of schistosomal granulomas. The serum antigen was absent, while the serum antibody was detectable at low titre. At 12th weeks PI, there was a more statistically significant decrease in gastro-intestinal transit, and increase in the colonic muscle contractility. The colon was still inflamed, but the granulomas were reduced in size and in number, with increase in the fibrocytes density. These alterations coincided with absence of serum antigen and increase in the antibody titre. All changes were more pronounced in the 2nd group of mice (200 ceraria/mouse) than the 1st one (50 cercaria/mouse). So, intestinal schistosomiasis is associated with great structural, functional and immunological changes, related to the time course and the infection intensity which may be involved in the pathogenesis and clinical manifestations of the disease.

Trichuris muris resides in intimate contact with its host, burrowing within cecal epithelial cells. However, whether the enterocyte itself responds innately to T. muris is unknown. This study investigated for the first time whether colonic intestinal epithelial cells (IEC) produce cytokines or chemokines following T. muris infection and whether divergence of the innate response could explain differentially polarized adaptive immune responses in resistant and susceptible mice. Increased expression of mRNA for the proinflammatory cytokines gamma interferon (IFN-gamma) and tumor necrosis factor and the chemokine CCL2 (MCP-1) were seen after infection of susceptible and resistant strains, with the only difference in expression being a delayed increase in CCL2 in BALB/c IEC. These increases were ablated in MyD88-/- mice, and NF-kappaB p65 was phosphorylated in response to T. muris excretory/secretory products in the epithelial cell line CMT-93, suggesting involvement of the MyD88-NF-kappaB signaling pathway in IEC cytokine expression. These data reveal that IEC respond innately to T. muris. However, the minor differences identified between resistant and susceptible mice are unlikely to underlie the subsequent development of a susceptible type 1 (IFN-gamma-dominated) or resistant type 2 (interleukin-4 [IL-4]/IL-13-dominated) adaptive immune response.

Pathology of the colon in pigs infected with Trichuris suis and fed an inulin and a non-inulin containing diet was studied to investigate the inflammatory response induced and the influence of inulin on this. Twenty-nine pigs were allocated into four groups (N-7, I-7, N-9 and N/I-9). Groups N-7, N-9 and N/I-9 were given a diet with non-fermentable carbohydrates, and group I-7 was fed a diet including fermentable carbohydrates (inulin). After 2 weeks, all pigs were inoculated with 2000 T. suis eggs. Seven weeks post-infection (p.i.), groups N-7 and I-7 were killed and group N/I-9 changed to inulin diet to study the influence of inulin on already established T. suis. Nine weeks p.i., groups N-9 and N/I-9 were killed. Trichuris suis were collected from the colon for enumeration. Tissues from the colon of each pig were taken for histological and immunohistochemical quantitative and semi-quantitative evaluations of heterophils, eosinophils, mast cells, IgA(+), IgG(+), IgM(+) and CD3(+) cells. The findings were compared with tissues from seven uninfected pigs of the same age. Pigs fed inulin had significantly fewer worms compared with pigs on the non-fermentable carbohydrate diet. The number of inflammatory cells in the colonic mucosa was increased in all T. suis-infected pigs compared with uninfected controls. The numbers of eosinophils, mast cells, IgA(+), IgG(+) and CD3(+) cells were significantly lower in pigs fed inulin than pigs fed non-fermentable carbohydrate. Whether this is a direct effect of inulin or a secondary effect due to the lower parasitic burden in inulin fed pigs is not known.

Entamoeba histolytica is a protozoan intestinal parasite that causes amoebic colitis and amoebic liver abscess. To identify virulence factors of E. histolytica, we first defined the phenotypes of two E. histolytica strains, HM-1:IMSS, the prototype virulent strain, and E. histolytica Rahman, a strain that was reportedly less virulent than HM-1:IMSS. We found that compared with HM-1:IMSS, Rahman has a defect in erythrophagocytosis and the ability to cause amoebic colitis in human colonic xenografts. We used differential in-gel 2D electrophoresis to compare the proteome of Rahman and HM-1:IMSS, and identified six proteins that were differentially expressed above a fivefold level between the two organisms. These included two proteins with antioxidative properties (peroxiredoxin and superoxide dismutase), and three proteins of unknown function, grainin 1, grainin 2 and a protein containing a LIM-domain. Overexpression of peroxiredoxin in Rahman rendered the transgenic trophozoites more resistant to killing by H2O2 in vitro, and infection with Rahman trophozoites expressing higher levels of peroxiredoxin was associated with higher levels of intestinal inflammation in human colonic xenografts, and more severe disease based on histology. In contrast, higher levels of grainin appear to be associated with a reduced virulence phenotype, and E. histolytica HM-1:IMSS trophozoites infecting human intestinal xenografts show marked decreases in grainin expression. Our data indicate that there are definable molecular differences between Rahman and HM-1:IMSS that may explain the phenotypic differences, and identify peroxiredoxin as an important component of virulence in amoebic colitis.

In order for the protozoan parasite Entamoeba histolytica (E.h.) to cause invasive intestinal and extraintestinal infection, which leads to significant morbidity and mortality, it must disrupt the protective mucus layer by a previously unknown mechanism. We hypothesized that cysteine proteases secreted from the amoeba disrupt the mucin polymeric network, thereby overcoming the protective mucus barrier. The MUC2 mucin is the major structural component of the colonic mucus gel. Heavily O-glycosylated and protease-resistant mucin domains characterize gel-forming mucins. Their N- and C-terminal cysteine-rich domains are involved in mucin polymerization, and these domains are likely to be targeted by proteases because they are less glycosylated, thereby exposing their peptide chains. By treating recombinant cysteine-rich domains of MUC2 with proteases from E.h. trophozoites, we showed that the C-terminal domain was specifically targeted at two sites by cysteine proteases, whereas the N-terminal domain was resistant to proteolysis. The major cleavage site is predicted to depolymerize the MUC2 polymers, thereby disrupting the protective mucus gel. The ability of the cysteine proteases to dissolve mucus gels was confirmed by treating mucins from a MUC2-producing cell line with amoeba proteases. These findings suggest a major role for E.h. cysteine proteases in overcoming the protective mucus barrier in the pathogenesis of invasive amoebiasis. In this report, we identify a specific cleavage mechanism used by an enteric pathogen to disrupt the polymeric nature of the mucin gel.

A genome-wide transcriptional analysis of Entamoeba histolytica was performed on trophozoites isolated from the colon of six infected mice and from in vitro culture. An Affymetrix platform gene expression array was designed for this analysis that included probe sets for 9435 open reading frames (ORFs) and 9066 5' and 3' flanking regions. Transcripts were detected for > 80% of all ORFs. A total of 523 transcripts (5.2% of all E. histolytica genes) were significantly changed in amebae isolated from the intestine on Days 1 and 29 after infection: 326 and 109 solely on Days 1 and 29, and 88 on both days. Quantitative real-time reverse transcriptase PCR confirmed these changes in 11/12 genes tested using mRNA isolated from an additional six mice. Adaptation to the intestinal environment was accompanied by increases in a subset of cell signaling genes including transmembrane kinases, ras and rho family GTPases, and calcium binding proteins. Significant decreases in mRNA abundance for genes involved in glycolysis and concomitant increases in lipases were consistent with a change in energy metabolism. Defense against bacteria present in the intestine (but lacking from in vitro culture) was suggested by alterations in mRNA levels of genes similar to the AIG1 plant antibacterial proteins. Decreases in oxygen detoxification pathways were observed as expected in the anaerobic colonic lumen. Of the known virulence factors the most remarkable changes were a 20-35-fold increase in a cysteine proteinase four-like gene, and a 2-3-fold decrease in two members of the Gal/GalNAc lectin light subunit family. Control of the observed changes in mRNA abundance in the intestine might potentially rest with four related proteins with DNA binding domains that were down-regulated 6-16-fold in the intestinal environment. In conclusion, the first genome-wide analysis of the transcriptome of E. histolytica demonstrated that the vast majority of genes are transcribed in trophozoites, and that in the host intestine trophozoites altered the expression of mRNAs for genes implicated in metabolism, oxygen defense, cell signaling, virulence, antibacterial activity, and DNA binding.

The clinical and microscopic appearances of inflammatory bowel disease may be very similar to those of amebic colitis. The coexistence of invasive amebiasis with inflammatory bowel disease may have disastrous results. Patients with inflammatory bowel disease have a greater prevalence of amebiasis, but this association is more significant for ulcerative colitis. There have been very few reports in the literature presenting the superimposition of amebiasis on Crohn's disease. In this report, a rare case of Crohn's colitis with superimposed amebiasis resulting in colonic perforation is presented. Patients with inflammatory bowel disease traveling to endemic areas may benefit from receiving a course of prophylactic anti-amebic medication.

Life cycle of Eimeria krijgsmanni-like coccidium isolated from the feces of naturally infected mice purchased from commercial sources was examined. The parasite was purified by single oocyst isolation and maintained by passage in the mice before experiments. The sporulated oocysts were ovoid or ellipsoid, measuring 19.3 x 14.8 microm on average. One or two small polar granules were present. Micropyle and oocyst residuum were absent. Sporocysts were ellipsoid, measuring 11.6 x 7.2 microm on average with a small Stieda body and sporocyst residuum. Six groups of respective 5 mice (4-week-old) were inoculated with doses varying from 2.0 x 10(1) to 10(6) oocysts. All the mice examined began to shed oocysts from 7 day postinoculation (PI) and their maximum number of oocysts per gram of feces were 10(6) on day 8 PI. Patency was 6 or 7 days. This parasite had severe virulence to the mice that is, the mice given 10(6) oocysts showed anorexia, diarrhoea and rough hair from 1 day and all of them died on day 3 PI. The mice given 10(3) or more oocysts showed the clinical signs described above from day 5 and 4 of them received 10(5) died on day 9 or 10 PI. The parasites occurred within the epithelial cells of cecum, colon and rectum of infected mice. Sporozoites, 13.9 x 3.0 microm, with two large refractil bodies on side of the nucleus located subcentrally were observed on day 1 and 2 PI. Merozoites were first observed at 24 hr PI, and sexual stages were found from 4 day PI. No parasites were detected in the small intestine and mecenteric lymph nodes.

Nematodes from the ventral colon of 31 adult horses, 24 males and 9 females, in the metropolitan region of the state of Rio de Janeiro were analysed. There were 53,444 (86.4%) adults of the total recovered strongylid nematodes. They belonged to 21 species of Cyathostominae and seven of Strongylinae. Larval forms made up 13.6% (8407) of the total recovered, and 49% of the strongylid nematodes were observed in ventral colon. The most prevalent and abundant species were Cyathostomum tetracanthum, Cylicocyclus nassatus, Cylicostephanus minutus, Cylicostephanus longibursatus, Cylicostephanus leptostomus, Cylicostephanus calicatus and Cylicostephanus goldi, corresponding to 93.2% of the total adult population; these species were classified as central species, except C. goldi; and other species were classified as secondary (n = 8) and satellite (n = 14). The low Green's aggregation index, presented to central species, indicated high dispersion because they were found in a greater number of infracommunities and were proven by the greater prevalence. Only 12.1% of the horses were uninfected or infected by a single species; the other infections were multiple, ranging from 3 to 23 species.

A 65-year old Korean man, living in Mokpo-city, Jeollanam-do, Republic of Korea, visited a local clinic complaining of right upper quadrant pain and indigestion. At colonoscopy, he was diagnosed as having a carcinoma of the ascending colon, and thus, a palliative right hemicolectomy was performed. Subsequently, an adult fluke of Gymnophalloides seoi was incidentally found in a surgical pathology specimen of the lymph node around the colon. The worm was found to have invaded gut lymphoid tissue, with characteristic morphologies of a large oral sucker, a small ventral sucker, and a ventral pit surrounded by strong muscle fibers. This is the first reported case of mucosal tissue invasion by G. seoi in the human intestinal tract.

Tritrichomonas foetus is a venereal pathogen of naturally bred cattle. In domestic cats, T. foetus colonizes the colon, resulting in chronic, large-bowel diarrhea. The infection is prevalent among young, densely housed cats, and there is no effective treatment. To the authors' knowledge, the characteristic microscopic lesions of T. foetus infection in naturally infected cats have not been described. The aim of the study reported here was to characterize the histologic changes in the colon of seven cats with T. foetus infection and chronic diarrhea. All cats were 1 year old or younger (mean, 6.7 +/- 1.7 months), and a diagnosis of T. foetus infection was made on the basis of direct fecal smear examination (five cats), fecal culture in InPouch TF medium (four cats), single-tube nested polymerase chain reaction (PCR) analysis of DNA extracted from feces (two cats), or observation of trichomonads in sections of colon followed by PCR confirmation on DNA extracted from paraffin-embedded tissue (two cats). The presence of colonic trichomonads was the most diagnostic histologic feature. Organisms were identified in all cats, but in only 24 of 43 (56%) sections of colon. Trichomonads were generally present in close proximity to the mucosal surface and less frequently in the lumen of colonic crypts. The presence of colonic trichomonads was consistently associated with mild-to-moderate lymphoplasmacytic and neutrophilic colitis, crypt epithelial cell hypertrophy, hyperplasia and increased mitotic activity, loss of goblet cells, crypt microabscesses, and attenuation of the superficial colonic mucosa. In two of the cats, histologic lesions were more severe and were associated with invasion of trichomonads into the lamina propria and/or deeper layers of the colon.

The DNA content of Entamoeba parasites appears to be regulated by an unusual mechanism. This conclusion, however, was based on experiments that examined parasites grown in media that did not contain short chain fatty acids (SCFAs) normally found in the colonic lumen. Since one of these SCFAs, butyrate, is known to affect DNA replication in eukaryotic cells, we examined the effect of SCFAs on Entamoeba trophozoite DNA content. Similar to reports from others, we found that Entamoeba invadens trophozoite cultures grown in conventional medium (TYI-S-33) contained cells with 2N, 4N, 8N, and 16N amounts of DNA. In contrast, cultures grown in TYI medium containing colonic SCFAs added in place of glucose contained a minor population with 2N, a major population with 4N, and very few cells with higher amounts of DNA. SCFAs also prevented the normal increase in the number of nuclei per cell in trophozoites that were induced to encyst. These results suggest that E. invadens trophozoite stage parasites growing in the intestine in the presence of high amounts of SCFAs have a ploidy range restricted to 2N/4N. Axenic growth of trophozoites in the absence of SCFAs, however, appears to allow trophozoites to increase the amount of DNA per cell, which they must do during the normal encystment process.

Degradation of the mucus layer by Entamoeba histolytica is a prerequisite for invasion of the colonic mucosa. In this study, we demonstrate that amoeba-secreted products degrade (3)H-labeled and native colonic mucin oligosaccharides independently of proteolytic activity. We conclude that E. histolytica degrades mucin oligosaccharides, which may facilitate parasite invasion of the colon.

History and Admission Findings: A 65-year-old woman was admitted to hospital with abdominal discomfort for several years. Travel history revealed two 4-week stays in Mwanza/Tanzania 15 and 17 years earlier., Investigations: Laboratory tests showed eosinophilia and an increase of IgE and antibodies against Schistosoma mansoni (IHA, EIA). Stool was negative for worm eggs. Colonoscopy revealed in several parts small nodules and increased vascularisation. Histology showed granulomas and eggs of Schistosoma mansoni., Treatment and Course: Anthelmintic therapy with praziquantel was given. After that the patient was well. One year later, follow-up endoscopy and histology were the same as previously. Another course of Praziquantel was given. A year later the patient was still well., Conclusion: Even after several years the rare case of intestinal schistosomiasis should be considered in patients with a history of travel in endemic regions. In case of negative stool specimen biopsies of the colon and rectum should be taken.

Two evolutionary lineages, called Trypanosoma cruzi I and II, have been identified in T. cruzi, the etiologic agent of human Chagas disease. Here, we describe a molecular strategy for direct genetic typing of these major groups of T. cruzi directly in human tissues. The protocol is based on heminested PCR amplification of the D7 region of the 24Salpha ribosomal DNA (rDNA), followed by identification of the products using denaturation curves in real time PCR. The repetitive nature of the gene, and the heminested PCR format insured the high sensitivity necessary to detect the presence of the very scarce T. cruzi DNA present in the chronically infected human tissues. There is 80% DNA sequence homology between the two 24Salpha rDNA alleles that define the T. cruzi I and II groups, sufficient to produce different thermal denaturation curves with melting temperature (TM) values of 81.7+/-0.43 and 78.2+/-0.33 degrees C (mean+/-SEM). Using this technical approach, we analysed tissue samples (esophagi, hearts and colon) from 25 different patients with the gastrointestinal or cardiac forms of Chagas disease; in all of them we found only the presence of T cruzi II. Previous epidemiological and immunological findings had already led to the idea that chronic human infections occurring in Brazil and Argentina might be primarily due to T. cruzi II strains, but all the evidence available had been indirect. Our findings provide definitive proof of this hypothesis and will also allow the establishment of which group of T. cruzi is responsible for Chagas disease in other countries.

Entamoeba parasites multiply as trophozoites in the layer of mucus that overlies the colonic epithelium. In response to stimuli that are not understood, trophozoites stop multiplying and differentiate into cysts that are released to infect another host. In the colon, Entamoeba trophozoites are exposed to the large variety of biochemicals that are carried into or are produced within this organ. The normal bacterial population of the colon releases large amounts of short-chain fatty acids (SCFAs). These compounds have effects on the growth, differentiation and repair of the colonic epithelium that correlate with de-creased activity of a Class I/II histone deacetylase (HDAC). We found that the formation of cysts, but not the growth of trophozoite-stage Entamoeba invadens parasites, was inhibited by physiologic concentrations of SCFAs. Variable levels of cyst formation did occur if SCFA concentrations were lowered. Specific inhibitors of Class I/II-type HDACs also prevented encystation, and trophozoites exposed to these compounds had increased levels of acetylation of histone H4 and other nuclear proteins. These results suggest that production of the infectious cyst stage of Entamoeba parasites is regulated in part by the levels of SCFAs made by the bacterial population of the colon.

Tetraphyllidean plerocercoids have occasionally been reported in marine mammals, but they have rarely been described in detail, and the ecological significance of these infections is unclear. We described plerocercoids collected from the mucosa of the terminal colon and rectum, the anal crypts, and the hepatopancreatic ducts of 7 striped dolphins Stenella coeruleoalba, 1 Cuvier's beaked whale Ziphius cavirostris, and 3 Risso's dolphins Grampus griseus from the Spanish Mediterranean. We also examined undescribed plerocercoids from 3 cetacean species from the Atlantic and the Pacific. All plerocercoids had a lanceolate body, and a scolex with an apical sucker and 4 sessile monolocular bothridia. The bothridia had free posterior edges and an accessory sucker at their anterior end. Under light microscopy, the bothridia of some Mediterranean specimens looked bilocular without accessory suckers, but a true accessory sucker was observed in histological sections. A principal component analysis revealed 2 stable clusters of specimens along the first principal component regardless of host species. These "large" and "small" morphotypes are thought to represent early migratory stages of Phyllobothrium delphini and Monorygma grimaldii. The similarity in scolex morphology, the observation of plerocercoids buried in intestinal regions close to the sites where M. grimaldii and P. delphini occur, and the coexistence of all larval forms in the same individual hosts would support this hypothesis. Future molecular analysis may confirm it.

The association between worm infections and bacterial diseases has only recently been emphasized. This study examined the effect of experimental Angiostrongylus costaricensis infection on endogenous intestinal flora of Swiss Webster mice. Eight mice aging six weeks were selected for this experiment. Four were infected with A. costaricensis and the other four were used as controls. Twenty eight days after the worm infection, all mice in both groups were sacrificed and samples of the contents of the ileum and colon were obtained and cultured for aerobic and anaerobic bacteria. In the mice infected with A. costaricensis there was a significant increase in the number of bacteria of the endogenous intestinal flora, accompanied by a decrease in the number of Peptostreptococcus spp. This alteration in the intestinal flora of mice infected by the nematode may help to understand some bacterial infections described in humans.

The present research analyses the reliability of coprological tests, both quantitative and qualitative, as indicators of the parasite burden of hosts, using data from wild boars (Sus scrofa) living in Livorno Mountain Park (Tuscany, Central Italy). In the case of intestinal strongyles, which turned out to be the dominant helminths of wild boars, the qualitative coprological test appears as a bad predictor of the real parasite situation of the herds, due to the high number of false negative results (34 animals out of 68). On the other hand, the positive predictive value of the test is high (90%). The quantitative test is significantly correlated with the individual parasite burden of wild boars.

Whipworms (Trichuris spp.) were identified in the colon of a recently purchased, 10-month-old dairy heifer that died suddenly. A skin test was positive for bovine viral diarrhea virus (BVDV). Signs of BVDV occurred in other heifers in the group, but fecal flotations were negative for whipworm eggs.

The clinical presentations of bacillary dysentery caused by shigella, and amoebic dysentery caused by the protozoan parasite Entamoeba histolytica, can be indistinguishable, with both organisms causing colonic mucosal damage and ulceration. However, the two organisms are quite distinct, and have very different pathogenic mechanisms. This raises the fundamental question of whether the similar clinical manifestations reflect a stereotypic response of the human gut to mucosal injury, or whether there are differences at the molecular level in the host response to individual gut pathogens. To characterize the human colonic response to each pathogen at the molecular level, we measured the differential transcription of nearly 40,000 human genes in sections of human colonic xenografts obtained 4 and 24 h following infection with Shigella flexneri or E. histolytica. Our results indicate that much of the human colonic response to these two pathogens is stereotypic, with increased expression of genes activated in cells undergoing stress and/or hypoxic responses, genes encoding cytokines, chemokines, and mediators that are involved in immune and inflammatory responses, and genes encoding proteins involved in responses to tissue injury and in tissue repair. The responses to amoeba and Shigella were not identical however, and we found unique elements in each response that may provide new insights into the distinct pathogenic mechanisms of E. histolytica and S. flexneri.

Amoebiasis is the second most common parasitic disease worldwIde. It occurs mainly in developing countries. A high percentage of people in countries where it is endemic are asymptomatic carriers. It results in severe disease that can be fatal in rare cases. Diabetics are at increased risk of exposure as travel to countries where it is endemic becomes more frequent, as indicated by the present case. This patient suffered from amoebiasis that produced an amoeboma which is most rare in cases of colonic amoebiasis. The clinical picture was that of an occluding gut tumor, but it was treated only with drugs. Retrospective studies show that diabetics are at increased risk of suffering severe complications after amoebic infection. The frequency and severity of this diabetes-amoeba association requires patients to take prophylactic measures, especially when travelling in developing countries.

The base line prevalence of Echinococcus multilocularis in foxes was determined in the eastern part of the province of Groningen in the Netherlands adjacent to the German border. This region has been identified in a previous study in 1998 as one of the westernmost border areas of E. multilocularis. Base line prevalence data are important for a better insight in the possible spread of the parasite and its changes in time. As fox feces containing E. multilocularis eggs are an important source for human exposure this base line prevalence is also an indicator for the potential risk for public health. The base line prevalence was estimated at 9.4% (95% CI: 5.2-16.5%). These results confirm previous findings of E. multilocularis in the same region. The spatial distribution of the infected foxes has been analyzed as a spatial gradient using a logistic model. The prevalence appeared to change strongest in east-western direction and was highest near the German border, adjacent to a German endemic area. These results suggest that the border areas in the Netherlands are the most margin of E. multilocularis territory.

Detection of Trichuris trichiura during colonoscopic examination is an unusual finding, at least in developed countries. We report a case of a coincidental endoscopic diagnosis of whipworm infestation performed in a patient referred to our open-access endoscopy even before a faecal examination for ova and/or parasites had been performed. Review of literature on colonoscopic diagnosis of T. trichuria is provided.

The nutritional basis of breakdown of immunity to parasites may be addressed in a rodent model. We hypothesized that lactating rats would show a breakdown of immunity to Nippostrongylus brasiliensis, and that this breakdown of immunity would be sensitive to protein supply. Rats were immunized with 1600 infective N. brasiliensis larvae and subsequently mated. During lactation, these rats were offered foods with 90 (low protein; LP) or 210 (high protein, HP) g crude protein (Nx6.25)/kg and re-infected with 400, 800 or 1600 larvae on day 2 post-parturition. Immunized non-reproducing rats were offered a food containing 60 g crude protein/kg and re-infected with 1600 larvae. Seven days after secondary infection, lactating rats had more adult nematodes in their small intestine and nematode eggs in their colon contents than the non-reproducing rats. Protein supply did not affect worm or egg counts, although LP rats carried relatively more female nematodes than the HP rats. All lactating rats had lower intakes than expected from previous studies using similar nutritional protocols. This may have resulted in insufficient protein supply, even for the HP rats, and this could explain the absence of effects of protein supply on egg and worm counts. We conclude that a breakdown of immunity to N. brasiliensis can occur in lactating rats; this strongly suggests that the lactating rat is a suitable model for elucidating a possible nutritional basis of breakdown of immunity to parasites. However, sufficient protein intake must be achieved to address the hypothesis that breakdown of immunity to N. brasiliensis is sensitive to protein supply.