Giardia Lamblia Subtypes and Their Relationship with Clinical Symptoms in Patients with Giardiasis.

Giardia lamblia has proved to be the most common intestinal protozoan parasite in humans that causes giardiasis. Given the high mutations in the genome of this parasite, the present study was conducted to determine the prevalence of Giardia lamblia subtypes and their relationship with clinical symptoms in patients who appear to have giardiasis. In 69 stool specimens with an appropriate number of giardia cysts, the DNA was first purified, and the genotype was then determined based on the glutamate dehydrogenase (gdh) gene sequence using PCR-RFLP. Data were collected on the clinical symptoms of the patients through a questionnaire, and their relationship with molecular results was studied. Four samples (5.8%) were found to be of subtype AI, 51 (73.9%) of subtype AII and 14 (20.3 %) of subtype BIII. No BIV subtype was found in the present study. A correlation was observed between Giardia lamblia genotypes (AI, AII and BIII) and abdominal pain. All of the people (100%) who had the AI genotype (i.e. the zoonosis subtype) had been losing weight. There was a significant correlation between weight loss and the AI subtype. All of the people (100%) infected with the BIII genotype experienced diarrhea, and this genotype was found to be associated with diarrhea. The present study found abdominal pain to be the most common symptom of giardiasis in Ilam province. Moreover, humans were found to be the main reservoir for giardia lamblia, although zoonosis subtypes such as AI and BIII still exist in the region and pose a risk for a giardiasis epidemic.

Exacerbated symptoms in Blastocystis sp.-infected patients treated with metronidazole: two case studies.

Blastocystis sp. is a gastrointestinal (GI) protozoan parasite reported to cause non-specific GI symptoms including diarrhea, flatulence, abdominal pain, and nausea. Complete eradication of Blastocystis sp. is rather challenging even with the drug of choice, i.e., metronidazole. Here, we report on two Blastocystis sp.-infected individuals, who presented increased parasite load and exacerbated symptoms upon treatment with the usual recommended dosage and regime of metronidazole. The two studies uniquely demonstrate for the first time a cyst count as high as fivefold more than the original cyst count before treatment and show an exacerbation of GI symptoms despite treatment. The study provides additional support in recognizing metronidazole resistance in Blastocystis sp. and its consequences towards the pathogenicity of the parasite.

Disease severity in patients with visceral leishmaniasis is not altered by co-infection with intestinal parasites.

Visceral leishmaniasis (VL) is a neglected tropical disease that affects the poorest communities and can cause substantial morbidity and mortality. Visceral leishmaniasis is characterized by the presence of Leishmania parasites in the spleen, liver and bone marrow, hepatosplenomegaly, pancytopenia, prolonged fever, systemic inflammation and low body mass index (BMI). The factors impacting on the severity of VL are poorly characterized. Here we performed a cross-sectional study to assess whether co-infection of VL patients with intestinal parasites influences disease severity, assessed with clinical and haematological data, inflammation, cytokine profiles and BMI. Data from VL patients was similar to VL patients co-infected with intestinal parasites, suggesting that co-infection of VL patients with intestinal parasites does not alter disease severity.

Intestinal parasites, growth and physical fitness of schoolchildren in poor neighbourhoods of Port Elizabeth, South Africa: a cross-sectional survey.

BACKGROUND: As traditional lifestyle and diets change with social and economic development, disadvantaged communities in low- and middle-income countries increasingly face a double burden of communicable and non-communicable diseases. We studied the relationship between physical fitness and infections with soil-transmitted helminths (STHs), intestinal protozoa and Helicobacter pylori among schoolchildren in Port Elizabeth, South Africa. METHODS: We conducted a cross-sectional survey among 1009 children, aged 9 to 12 years, from eight primary schools in socioeconomically disadvantaged neighbourhoods of Port Elizabeth. Physical fitness was determined using field-deployable tests of the Eurofit fitness test battery. Stool samples were analysed with the Kato-Katz thick smear technique to diagnose STHs and with rapid diagnostic tests (RDTs) to detect intestinal protozoa and H. pylori infections. Haemoglobin (Hb) levels were assessed and anthropometric indicators determined. RESULTS: Complete data were available for 934 children (92 %). In two schools, high STH prevalences were found (Ascaris lumbricoides 60 and 72 %; Trichuris trichiura 65 % each). For boys and girls co-infected with A. lumbricoides and T. trichiura (n = 155) the maximal oxygen uptake (VO2 max) was estimated to be 50.1 and 47.2 ml kg(-1) min(-1), compared to 51.5 and 47.4 ml kg(-1) min(-1) for their non-infected peers (n = 278), respectively. On average, children without helminth infections had greater body mass (P = 0.011), height (P = 0.009) and a higher body mass index (P = 0.024) and were less often stunted (P = 0.006), but not significantly less wasted compared to their peers with a single or dual species infection. Among 9-year-old boys, a negative correlation between helminth infections and VO2 max, grip strength and standing broad jump distance was observed (P = 0.038). The overall mean Hb level was 122.2 g l(-1). In the two schools with the highest prevalence of STHs the Hb means were 119.7 and 120.5 g l(-1), respectively. CONCLUSIONS: Intestinal parasite infections appear to have a small but significant negative effect on the physical fitness of infected children, as expressed by their maximal oxygen uptake. We observed a clear impact on anthropometric indicators.

Parasitosis y síndrome de intestino irritable / Parasitosis and irritable bowel syndrome

El síndrome de intestino irritable (SII) es un trastorno funcional digestivo de etiología multifactorial. En su fisiopatología se describen diversos factores, tanto biológicos, como psicológicos y ambientales, que afectan el estado de activación de células inmunes en la mucosa intestinal. Entre los factores ambientales se incluye la presencia de alguna parasitosis intestinal. El síndrome de intestino irritable post-infeccioso (SII-PI) es reconocido como un subgrupo de estos trastornos, cuya aparición de los síntomas es posterior a una infección intestinal provocada por agentes microbianos. A pesar de que en Chile hay pocos estudios respecto a la relación entre SII y parasitosis intestinal, se ha descrito la existencia de una asociación positiva entre SII e infecciones por Blastocistis hominis, uno de los parásitos prevalentes en Chile. En otros países, se ha descrito además una relación entre SII, amebiasis y giardiasis. Por la alta prevalencia de parasitosis en nuestro país, existe la necesidad de ampliar los estudios para clarificar la fuerza de la asociación entre parasitosis y SII.

Irritable bowel syndrome (IBS) is a functional disorder of the gastrointestinal tract characterised by multi-factorial aetiology. In IBS physiopathology are involved diverse factors between them biological, psychosocial, and environmental components which affect the immune activation status of gut mucosa. Among these factors is recognized the intestinal parasitosis. Post-infection IBS (PI-IBS) is recognised as a subgroup of functional disorders whose symptoms onset appear after a symptomatic intestinal infection caused by microbial agents. There are few studies regarding of relationship between IBS and intestinal parasitosis in Chile. However, is has been well described a positive association between IBS and Blastocystis hominis infections, one of prevalent parasites in Chile. In other countries, is also described a relationship between IBS and amebiasis and giardiasis. Both, characterized by a common mode of transmission through water as well as contaminated food. Because the high prevalence of parasitosis in our country it is necessary to expand the association studies to clarify the strength of the parasites ethiology in IBS.

Increased intestinal epithelial cell turnover and intestinal motility in Gymnophalloides seoi-infected C57BL/6 mice.

The changing patterns of goblet cell hyperplasia, intestinal epithelial cell turnover, and intestinal motility were studied in ICR and C57BL/6 mice infected with Gymnophalloides seoi (Digenea: Gymnophallidae). Whereas ICR mice retained G. seoi worms until day 7 post-infection (PI), C57BL/6 mice showed a rapid worm expulsion within day 3 PI. Immunosuppression with Depo-Medrol significantly delayed the worm expulsion in C57BL/6 mice. Goblet cell counts were increased in both strains of mice, peaking at day 1 PI in C57BL/6 mice and slowly increasing until day 7 PI in ICR mice. In C57BL/6 mice infected with G. seoi, newly proliferating intestinal epithelial cells were remarkably increased in the crypt, and the increase was the highest at day 1 PI. However, in ICR mice, newly proliferating intestinal epithelial cells increased slowly from day 1 to day 7 PI. Intestinal motility was increased in G. seoi-infected mice, and its chronological pattern was highly correlated with the worm load in both strains of mice. Meanwhile, immunosuppression of C57BL/6 mice abrogated the goblet cell proliferation, reduced the epithelial cell proliferation, and suppressed the intestinal motility. Goblet cell hyperplasia, increased intestinal epithelial cell turnover, and increased intestinal motility should be important mucosal defense mechanisms in G. seoi-infected C57BL/6 mice.

Effect of deworming vs Iron-Folic acid supplementation plus deworming on growth, hemoglobin level, and physical work capacity of schoolchildren.

The effect of deworming vs deworming and weekly Iron-Folic acid (IFA) on growth, hemoglobin level, and physical work capacity of children was studied. Children from three rural schools studying from 4th to 7th standard were selected. One set of school children were given deworming tablet (400 mg albendezole) once in six months while the second school children received deworming tablet along with weekly dose of Iron Folic acid Tablet (60 mg of elemental iron and 0.5 mg folic acid). Anthropometric measurements, hemoglobin, and physical work capacity was estimated. No significant change was noticed in the prevalence of malnutrition or physical work capacity of the children. As compared to only deworming, IFA + Deworming showed 17.3% increase in the hemoglobin levels (P<0.001). Thus weekly IFA along with deworming has shown beneficial effect on the hemoglobin levels of the children.

Genetic hemoglobin disorders, infection, and deficiencies of iron and vitamin A determine anemia in young Cambodian children.

In Cambodia, many factors may complicate the detection of iron deficiency. In a cross-sectional survey, we assessed the role of genetic hemoglobin (Hb) disorders, iron deficiency, vitamin A deficiency, infections, and other factors on Hb in young Cambodian children. Data on sociodemographic status, morbidity, and growth were collected from children (n = 3124) aged 6 to 59 mo selected from 3 rural provinces and Phnom Penh municipality. Blood samples were collected (n = 2695) for complete blood count, Hb type (by DNA analysis), ferritin, soluble transferrin receptor (sTfR), retinol-binding protein (RBP), C-reactive protein, and α(1)-acid glycoprotein (AGP). Genetic Hb disorders, anemia, and vitamin A deficiency were more common in rural than in urban provinces (P < 0.001): 60.0 vs. 40.0%, 58.2 vs. 32.7%, and 7.4 vs. 3.1%, respectively. Major determinants of Hb were age group, Hb type, ferritin, sTfR, RBP, AGP >1.0 g/L (P < 0.001), and rural setting (P < 0.05). Age group, Hb type, RBP, elevated AGP, and rural setting also influenced ferritin and sTfR (P < 0.02). Multiple factors affected anemia status, including the following: age groups 6-11.99 mo (OR: 6.1; 95% CI: 4.3, 8.7) and 12-23.99 mo (OR: 2.7; 95% CI: 2.1, 3.6); Hb type, notably Hb EE (OR: 18.5; 95% CI: 8.5, 40.4); low ferritin (OR: 3.2; 95% CI: 2.2, 4.7); elevated AGP (OR: 1.4; 95% CI: 1.2,1.7); rural setting (OR: 2.3; 95% CI: 1.7, 3.1); low RBP (OR: 3.6; 95% CI: 2.2, 5.9); and elevated sTfR (OR: 2.1; 95% CI: 1.7, 2.7). In Cambodia, where a high prevalence of genetic Hb disorders exists, ferritin and sTfR are of limited use for assessing the prevalence of iron deficiency. New low-cost methods for detecting genetic Hb disorders are urgently required.

Genes associated with alternatively activated macrophages discretely regulate helminth infection and pathogenesis in experimental mouse models.

Resolution of helminth infections is typically associated with the host launching a TH2 dominated immune response. In experimental models of helminth infections a key feature of this TH2 immunity is the induction of alternatively activated macrophage (AAM) populations. The importance of AAMs in immunity to helminths has initially been highlighted by the fact that their presence is essential for host survival from schistosomiasis. Since then it has become apparent that AAMs also play important roles in regulating the pathology and expulsion in a number of nematode infections. In the present review, we describe the diverse and complex roles of AAMs in regulating helminth infections and pathology. From these studies important findings are emerging on the functions of particular genes upregulated in AAM.

Elevated levels of urinary hydrogen peroxide, advanced oxidative protein product (AOPP) and malondialdehyde in humans infected with intestinal parasites.

Oxidative stress has been implicated as an important pathogenic factor in the pathophysiology of various life-threatening diseases such as cancer, cardiovascular diseases and diabetes. It occurs when the production of free radicals (generated during aerobic metabolism, inflammation, and infections) overcome the antioxidant defences in the body. Although previous studies have implied that oxidative stress is present in serum of patients with parasitic infection there have been no studies confirming oxidative stress levels in the Malaysian population infected with intestinal parasites. Three biochemical assays namely hydrogen peroxide (H2O2), lipid peroxidation (LP) and advanced oxidative protein product (AOPP) assays were carried out to measure oxidative stress levels in the urine of human subjects whose stools were infected with parasites such as Blastocystis hominis, Ascaris, Trichuris, hookworm and microsporidia. The levels of H2O2, AOPP and LP were significantly higher (P<0.001, P<0.05 and P<0.05 respectively) in the parasite-infected subjects (n=75) compared to the controls (n=95). In conclusion, the study provides evidence that oxidative stress is elevated in humans infected by intestinal parasites. This study may influence future researchers to consider free radical-related pathways to be a target in the interventions of new drugs against parasitic infection and related diseases.

Mechanisms of intestinal tight junctional disruption during infection.

Tight junctions are dynamic structures that may undergo structural and functional changes in response to both physiological and pathological circumstances. Several microbial pathogens impair intestinal barrier function by exploiting tight junctions. These pathogens have developed a broad and complex range of strategies to subvert host tight junction barrier function. The purpose of this review is to give an overview of the mechanisms whereby select enteric viruses, bacterial pathogens and parasites modulate intestinal tight junctional structure and function and how these effects may contribute to the development of chronic intestinal disorders.

Effect of chronic Giardia lamblia infection on epithelial transport and barrier function in human duodenum.

BACKGROUND: Giardia lamblia causes infection of the small intestine, which leads to malabsorption and chronic diarrhoea. AIM: To characterise the inherent pathomechanisms of G lamblia infection. METHODS: Duodenal biopsy specimens from 13 patients with chronic giardiasis and from controls were obtained endoscopically. Short-circuit current (I(SC)) and mannitol fluxes were measured in miniaturised Ussing chambers. Epithelial and subepithelial resistances were determined by impedance spectroscopy. Mucosal morphometry was performed and tight junction proteins were characterised by immunoblotting. Apoptotic ratio was determined by terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labelling staining. RESULTS: In giardiasis, mucosal surface area per unit serosa area was decreased to 75% (3%) of control, as a result of which epithelial resistance should increase. Instead, epithelial resistance of giardiasis biopsy specimens was decreased (19 (2) vs 25 (2) Omega cm(2); p<0.05) whereas mannitol flux was not significantly altered (140 (27) vs 105 (16) nmol/h/cm(2)). As structural correlate, reduced claudin 1 expression and increased epithelial apoptosis were detected. Furthermore, basal I(SC) increased from 191 (20) in control to 261 (12) microA/h/cm(2) in giardiasis. The bumetanide-sensitive portion of I(SC) in giardiasis was also increased (51 (5) vs 20 (9) microA/h/cm(2) in control; p<0.05). Finally, phlorizin-sensitive Na(+)-glucose symport was reduced in patients with giardiasis (121 (9) vs 83 (14) microA/h/cm(2)). CONCLUSIONS: G lamblia infection causes epithelial barrier dysfunction owing to down regulation of the tight junction protein claudin 1 and increased epithelial apoptoses. Na(+)-dependent d-glucose absorption is impaired and active electrogenic anion secretion is activated. Thus, the mechanisms of diarrhoea in human chronic giardiasis comprise leak flux, malabsorptive and secretory components.

Risk of cancer onset in sub-Saharan Africans affected with chronic gastrointestinal parasitic diseases.

Gastrointestinal Schistosomiasis and Amebiasis are uncommon in the western world, while such infections are frequent in the African community. In addition to the problems associated with the clinical symptoms of these parasitic infections, it is important to stress the increase in cancer of the Gastro-Intestinal (GI) tract. In this study we evaluate the prevalence of cancer in patients affected by chronic inflammatory diseases caused by the above named parasites. In three years, from January 2000 to December 2003, we observed a total of 1199 subject. Of these, 950 presented with complaints of diarrhoea, vomiting, abdominal pain, melena, hematemesis, rectal discharges and alteration of bowel habits. A total of 818 patients were evaluated in Uganda (Mulago and Arua hospitals) and 381 at Luisa Guidotti Hospital in Zimbabwe. An exhaustive clinical history was collected for each patient and then physical and laboratory examinations were performed. The clinical files of all patients previously admitted to the respective hospitals were obtained and the information taken from these files was then integrated with our clinical findings. Subjects who were found free of gastro-intestinal disease after examinations and did not have a clinical history of infective GI disease but presented with other pathologies, were regarded as control group. The control group was composed of 249 subjects. The subjects who were positive on examination underwent further investigations. The number of patients affected by schistosomiasis and amebiasis were 221 and 224 respectively. The number of patients who suffered from aspecific enterocolitis was 454, intestinal tuberculosis was present in 21 patients and we found 30 patients with esophageal candidiasis. Patients who had the above mentioned GI diseases were then divided into 3 groups. First group was composed of patients who had a clinical history of infective GI diseases and were re-admitted for similar symptoms, and on examination were positive for the presence of the same infective GI diseases. Such patients were placed in the Chronic group. The second group was formed of patients who had previously undergone treatment for infective GI diseases but on readmission were found free of infective GI disease, and this group was described as the Cured group. They had symptoms associated with other pathologies. A third group, which we described as the Acute group was composed of patients who did not have any previous case of GI infection and were admitted for the first time. Such patients were found positive on examination for infective GI diseases. In the 950 patients, we found a total of 45 tumors. The tumors were prevalent (42 tumors) in the chronic group. In 34 patients the tumor was in the colo-rectal region, in 3 patients in the stomach, in 4 patients in the esophagus and 1 patient had cancer in the small bowel. Our results show a strong association between the chronic infection of the GI tract and the likelihood to develop tumors. However, it is not clear which biological mechanisms are implicated in such transformations. They may depend on the chronic inflammation of the GI mucous which permits the entrance of carcinogenic materials or on the effects of mutagenic products produced by the parasites or both.

[Nitric oxide and anti-protozoan chemotherapy]. / L'ossido nitrico nella terapia anti-protozoaria.

Constitutive nitric oxide (NO) is generated by constitutively expressed types of NO-synthase enzymes (NOS-I and -III), being involved in physiological processes such as nervous transmission and vasodilatation. Inducible NO, synthesized by the NO-synthase isoform NOS-II, is an anti-pathogen and tumoricidal agent. However, inducible NO production requires a tight control because of cytotoxic and immune-modulation activity. NO produced by human and canine macrophages has long been demonstrated to be involved in the intracellular killing of Leishmania. Mechanisms of parasite survival and persistence in the host have been throughly investigated, and include suppression of NOS-II and the parasite entry into NOS-II negative cells. Both intracellular and extracellular morphotypes of Trypanosoma cruzi are killed by NO in vitro and in vivo, although a role of NO in the pathogenesis of heart disease has been reported. Killing of extracellular protozoa such as Trichomonas vaginalis and Naegleria fowleri by activated macrophages is also mediated by NO. The main control of Plasmodium spp infection in human and murine hepatocytes, and in human monocytes is achieved by NO-mediated mechanisms. Protection from severe malaria in African children has been found associated with polymorphisms of the NOS-II promoter; however, a pathogenic role of endogenous NO has been documented in cerebral malaria. Although several macromolecules are putative NO targets, recent experimental work has shown that NO-releasing compounds inhibit cysteine proteases (CP) of P. falciparum, T. cruzi and L. infantum in a dose-dependent manner. CPs are present in a wide range of parasitic protozoa and appear to be relevant in several aspects of the life cycle and of the parasite-host relationships. Comparative analysis of 3-D amino acid sequence models of CPs from a broad range of living organisms, from viruses to mammals, suggests that the Sy atom of the Cys catalytic residue undergoes NO-dependent chemical modification (S-nytrosilation and disulfide bridge formation), with the concomitant loss of enzyme activity. The NO-donor S-nitroso-N-acetilpenicillamine (SNAP) was shown to kill T. cruzi epimastigotes and L. infantum promastigotes in culture, while a combination of nitrite plus acid organic salts was highly effective against L. major amastigotes in mouse macrophages. A parasitostatic effect--with both encystation and excystation inhibition--of S-nitrosoglutathione and spermine-NONOate was documented in trophozoite cultures of Giardia duodenalis. Recently, a novel formulation of metronidazole bearing a NO-releasing group was found to enhance significantly the in vitro killing of Entamoeba histolytica trophozoites, compared to metronidazole. So far, only two clinical studies were performed on human patients, suffering from cutaneous leishmaniasis. In one study, 16 Ecuadorean patients were treated with a SNAP cream administered on lesions for 10 days. All lesions were parasitologically cured and clinically healed by day 30. In the second study, a different NO-producing cream (basically nitrite in acidic environment) was employed to treat 40 Syrian patients. Only 28% of them showed improvement and 12% were cured by day 60. In conclusion, despite the wide evidence that NO can be regarded as a natural anti-protozoal weapon, little efforts have been made to develop and test NO-based drugs in human medicine. This is mainly due to the difficulty in designing suitable chemical carriers able to release the right amount of NO, in the right place and in the right time, to avoid toxic effects against non-target host cells.

Neuronal nitric oxide synthase activity is increased during granulomatous inflammation in the colon and caecum of pigs infected with Schistosoma japonicum.

Neuronal nitric oxide is a non-adrenergic non-cholinergic neurotransmitter in the enteric nervous system and plays a role in a variety of enteropathies including Crohn's and Chagas' diseases, ulcerative colitis, diabetes, atrophy and hypertrophy. The content of neuronal nitric oxide synthase (nNOS) in the colon and the caecum from pigs infected with Schistosoma japonicum was studied using immunohistochemical and histochemical staining for nNOS and nicotinamide adenine dinucleotide phosphate diaphorase (NADPH-diaphorase), respectively. In the infected pigs, lightly, moderately and less severely inflamed tissues showed increased nNOS and NADPH-diaphorase activities in nerve cell bodies and nerve fibres in the enteric plexuses compared to control pigs. There was a significant increase in the nerve cell body density of nNOS immunoreactive nerve cell bodies in the inner submucous plexus, outer submucous plexus and in the myenteric plexus. More intensely stained nerve cell bodies and varicosities were observed in tissue from prenatally infected and prenatally infected, postnatally re-infected pigs compared to postnatally infected pigs. However, the latter showed the highest numerical density of nNOS immunoreactive nerve cell bodies. Marked increases were seen in the inner submucous plexus followed by myenteric plexus, inner circular muscle, outer submucous plexus and mucous plexus. However, in very severe inflamed tissues, the number and staining intensity of nerve cell bodies and nerve fibre varicosities were reduced in plexuses located in the lesions with the inner submucous and mucous plexuses being the most affected. There was no staining in the nervous tissue within the eosinophilic cell abscesses and productive granulomas. The apparent alterations in the activities of enzymes responsible for the generation of nitric oxide (NO) show possible alterations in the NO mediated non-adrenergic non-cholinergic reflexes in the enteric nervous tissue. These alterations might contribute to impaired intestinal motility and absorption, and other pathophysiological conditions seen during S. japonicum infections.

Intestinal regrowth is amplified after jejunal but not ileal resection during tapeworm infection in the rat.

The ileum possesses functions required by a healthy individual that are not fully supplanted by the duodenum or jejunum. Evidence suggests that the ileum may also be necessary to maintain an enteric parasite-host interaction. We hypothesized that the ileum is essential to the survival of the lumen-dwelling, rat tapeworm, H. diminuta. Male rats were divided into three groups: those with ileal or jejunal resections and nonresected controls. Half of each rat group was infected with the tapeworm. After jejunal resection, the weight but not length of intestinal remnant (duodenum + ileum) in infected rats returned to that of control, nonresected intestine 29 days after surgery and tapeworm numbers were fully maintained. In contrast, after ileal removal intestinal length and weight of the remaining duodenum and jejunum in infected rats were significantly decreased and tapeworm survival diminished. Data indicates that intestinal growth following resection is amplified by tapeworm infection when the ileum remains but diminished when the ileum is removed. Furthermore, loss of the ileum results in decreased infection intensity and dry weight of the tapeworm.

Impact of intestinal helminth infection on anemia and iron status during pregnancy: a community based study in Indonesia.

A cohort study was carried out in Purworejo District, Central Java, Indonesia to investigate prevalence of anemia and low iron stores during pregnancy in relation to intestinal helminth infection. 442 pregnant women were followed until 5-10 weeks postpartum, during the period of April 1996 - August 1998. Information on intestinal helminths, hemoglobin and serum ferritin was collected each trimester. Highest prevalence of anemia in pregnancy (37.1%) was found in the second trimester, while the highest prevalence of low iron stores (49.5%) was found in the third trimester. Most pregnant women (69.7%) were infected with at least one species of pathogenic intestinal helminths. The most common helminth detected was Trichuris trichiura followed by Necator americanus (hookworm) and Ascaris lumbricoides. A significant negative association was found between hookworm infection and serum ferritin at the first trimester (p = 0.010). It is concluded that hookworm infection can interfere iron stores. Other causes of anemia among pregnant women should be considered. Anthelminthic therapy could be given to infected women before conception as public health strategy to improve iron status.

Pathophysiology of amoebiasis.

Few organisms are more aptly named than Entamoeba histolytica, an intestinal protozoan parasite that can lyse and destroy human tissue. Within the past four years, new models of E. histolytica infection have begun to illuminate how amoebic trophozoites cause intestinal disease and liver abscess, and have expanded our understanding of the remarkable killing ability of this parasite. Here, I summarize recent work on the interactions between E. histolytica and human intestine, and between E. histolytica and hepatocytes, and discuss what these studies tell us about the role of inflammation and programmed cell death in the pathogenesis of amoebiasis.

Schistosoma mansoni infection causing diffuse enteric inflammation and damage of the enteric nervous system in the mouse small intestine.

Schistosomiasis mansoni is a major health problem, mainly occurring in developing countries. A large proportion of infected individuals suffers from motility-related gastrointestinal problems. In the present study, the diffuse inflammatory response in the small bowel wall, as compared to the egg-induced granulomatous inflammation, was investigated. For this purpose, OF1 mice infected with Schistosoma mansoni 8-16 weeks prior to the experiment, and uninfected control mice were studied. The ileum showed both a diffuse mucosal inflammation as well as a granulomatous reaction. The diffuse mucosal inflammation caused an increase in the thickness of the mucosa, with blunting of the villi. A significant, transient increase of thickness of the muscularis propria after 12 weeks of infection was noted. There was an infection-related mast cell infiltrate in the muscularis propria, consisting of formalin fixation-insensitive connective tissue mast cells. Ganglionitis of the myenteric plexus was noted. Rarely, ganglia of the myenteric plexus contained apoptotic cells. A general pharmacological set of experiments showed a significant increase in intestinal contractility, both to exogenously administered, as well as to endogenously released neurotransmitters. Our results demonstrate that S. mansoni infection in the mouse ileum leads to diffuse specific enteric inflammation that is associated with an enhanced response to contractile agents.