PREVALENCE OF INTESTINAL PARASITISM AND ASSOCIATED SYMPTOMATOLOGY AMONG HEMODIALYSIS PATIENTS

Intestinal parasites are an important cause of morbidity and mortality. Immunocompromised individuals may develop more severe forms of these infections. Taking into account the immunity impairment in patients suffering from chronic renal failure (CRF), we will determine the prevalence and associated symptoms of intestinal parasites in these patients. Controls without CRF were used for comparison. Stool samples were collected and processed for microscopic identification of parasites using the Formalin-ether concentration method. For Cryptosporidium diagnosis, the ELISA technique was used. One hundred and ten fecal samples from hemodialysis patients were analyzed, as well as 86 from a community group used as control group. A result of 51.6% of intestinal parasites was observed in hemodialysis patients and 61.6% in the control group. Cryptosporidium and Blastocystis were the most common infections in patients with CRF (26.4% and 24.5%, respectively). Blastocystis was the most common infection in the control group (41.9%), however no individual was found positive for Cryptosporidium. Among the CRF patients, 73.6% were symptomatic, 54.3% of these tested positive for at least one parasite, in contrast to 44.8% in asymptomatic patients (p = 0.38). The most common symptoms in this group were flatulence (36.4%), asthenia (30.0%) and weight loss (30.0%). In the control group, 91.9% were symptomatic, 60.8% of these tested positive for at least one parasite, in contrast to 71.4% in asymptomatic patients (p = 0.703). A significant difference between the two groups was observed with regard to symptoms, with bloating, postprandial fullness, and abdominal pain being more frequent in the control group than in the hemodialysis group (all p < 0.05). Comparing symptomatic with asymptomatic, there was no association in either group between symptoms or the prevalence of parasitic infection, nor with the type of parasite or with multiple parasitic infections. Patients with chronic renal failure are frequent targets for renal transplantation, which as well as the inherent immunological impairment of the disease itself, results in immunosuppression by medication. For this reason, carriers of intestinal parasites with pathogenic potential can develop serious clinical complications influencing the success of transplantation. This fact, coupled with the high prevalence of intestinal parasites and the dissociation between symptoms and infection in CRF patients, suggests that the stool test should be incorporated in routine propedeutics. Furthermore, preventive measures for the acquisition of parasites through the fecal-oral contamination route should be introduced.

PREVALENCE OF INTESTINAL PARASITES AMONG FOOD HANDLERS IN WESTERN IRAN

Parasitic infection is one of the problems that affect human health, especially in developing countries. In this study, all of the fast food shops, restaurants, and roast meat outlets of Khorramabad (Western Iran) and all the staff employed by them, some 210 people, were selected through a census and their stools were examined for the presence of parasites. The parasitological tests of direct wet-mount, Lugol's iodine staining, formaldehyde-ether sedimentation and Trichrome staining techniques were performed on the samples. The data was analyzed with a chi-square test and logistic regression was selected as the analytical model. The results showed 19 (9%) stool specimens were positive for different intestinal parasites. These intestinal parasites included Giardia lamblia2.9%, Entamoeba coli 4.3%, Blastocystis sp. 1.4%, and Hymenolepis nana 0.5%. There was a significant difference between the presence of a valid health card, awareness of transmission of intestinal parasites, participation in training courses in environmental health with intestinal parasites (p < 0.05). No statistically significant difference was found between the rate of literacy and gender among patients infected with intestinal parasites (p > 0.05). To control parasitic infection in food handlers, several strategies are recommended such as stool examinations every three months, public education, application of health regulations, controlling the validity of health cards and training on parasitic infection transmission. In this regard, the findings of the present study can be used as a basis to develop preventive programs targeting food handlers because the spread of disease via them is a common problem worldwide.

PREVALENCE OF INTESTINAL PARASITES AMONG FOOD HANDLERS OF SARI, NORTHERN IRAN

Parasitic infection is highly prevalent throughout the developing countries of the world. Food handlers are a potential source of infection for many intestinal parasites and other enteropathogenic infections as well. The aim of this study was to determine the prevalence of intestinal parasite carriers among food handlers attending the public health center laboratory in Sari, Northern Iran for annual check-up. The study was performed from August 2011 through February 2012. Stool samples were collected from 1041 male and female food handlers of different jobs aged between 18 to 63 years and were examined following standard procedures. Sociodemographic, environmental and behavioral data analysis of the food handlers were recorded in a separate questionnaire. Intestinal parasites were found in 161 (15.5%) of the studied samples. Seven species of protozoan or helminth infections were detected. Most of the participants were infected with Giardia lamblia (53.9%) followed by Blastocystis hominis (18%), Entamoeba coli (15.5%), Entamoeba histolytica/dispar (5.5%), Cryptosporidium sp. (3.1%), Iodamoeba butschlii (3.1%) and Hymenolepis nana (1.9%) as the only helminth infection. The findings emphasized that food handlers with different pathogenic organisms may predispose consumers to significant health risks. Routine screening and treatment of food handlers is a proper tool in preventing food-borne infections.

Absence of clinical abnormalities suggesting renal involvement during the long-term course of visceral Leishmaniasis

Abnormalities of renal function have been demonstrated inpatients with visceral leishmaniasis; although there was a trend toward normalization following antiparasitic therapy, some abnormalities persisted. With thepurpose of studying the long- term clinical course of renal involvement in visceral leishmaniasis, 32 patients with a diagnosis of this parasitic disease were evaluated in the endemic area and at least 6 months after the clinical cure of the disease and compared with a control group of 28 individuals. No patient had a history or clinical findings suggestive of renal disease and all were normotensive. Laboratory evaluation was normal in all except 3 patients with abnormal urinalysis. Mild proteinuria and microscopic hematuria were seen in a single urinalysis in one patient (although three other urinalysis were normal), and leucocyturia in two female patients. It was concluded that the renal involvement in visceral leishmaniasis is mild and transient, with normal renal function observed on long-term follow-up after cure of the parasitic infection.

Enteroparasites prevalence among daycare and elementary school children of municipal schools, Rolândia, PR, Brazil

Coproparasitological analyses were performed on 191 daycare children and 434 elementary school children from urban and rural areas in Rolândia, Parana State, Brazil. The overall prevalence of enteroparasites was 15.2 % for daycare children and 52.5% for elementary school children. Risk factors are discussed.

Relationship between protein-energy malnutrition, vitamin A, and parasitoses in children living in Brasília

It is still controversial whether intestinal parasitic infections can influence the nutritional status of children. The relationship between protein-energy malnutrition, vitamin A and parasitic infections was evaluated in 124 children. The food intake estimated by recall method was generally low and poor. Seventy five percent of the children were infected with intestinal parasites. The mean±SD weight-for-age and height-for-age Z-score were skewed one standard deviation to the left, when compared to normal standards. An association was found between protein-energy malnutrition and Giardia lamblia, but not with Ascaris lumbricoides or Hymenolepis nana infection. Only Giardia-infected children had a decreased weight-for-age and weight-for-height Z-score. Hypovitaminosis A was a major nutritional problem, but no relationship between this deficiency and parasitic infection was found. Our data indicate that low and poor food intake were the major cause of protein-energy malnutrition among the children, and except for Giardia, this was not influenced by parasitic infections.

Interaction of malaria parasites with host late endocytic and autophagic pathways is essential for Plasmodium liver stage development

RESUMO: A Malária é causada por parasitas do género Plasmodium, sendo a doença parasitária mais fatal para o ser humano. Apesar de, durante o século passado, o desenvolvimento económico e a implementação de diversas medidas de controlo, tenham permitido erradicar a doença em muitos países, a Malária continua a ser um problema de saúde grave, em particular nos países em desenvolvimento. A Malária é transmitida através da picada de uma fêmea de mosquito do género Anopheles. Durante a picada, os esporozoítos são injetados na pele do hospedeiro, seguindo-se a fase hepática e obrigatória do ciclo de vida. No fígado, os esporozoítos infetam os hepatócitos onde se replicam, dentro de um vacúolo parasitário (VP) e de uma forma imunitária silenciosa, em centenas de merozoitos. Estas novas formas do parasita são as responsáveis por infetar os eritrócitos, iniciando a fase sanguínea da doença, onde se os primeiros sintomas se manifestam, tais como a característica febre cíclica. A fase hepática da doença é a menos estudada e compreendida. Mais ainda, as interações entre o VP e os organelos da células hospedeira estão ainda pouco caracterizados. Assim, neste estudo, as interações entre os organelos endocíticos e autofágicos da célula hospedeira e o VP foram dissecados, observando-se que os anfisomas, que são organelos resultantes da intersecção do dois processos de tráfego intracelular, interagem com o parasita. Descobrimos que a autofagia tem também uma importante função imunitária durante a fase hepática inicial, ao passo, que durante o desenvolvimento do parasita, já numa fase mais tardia, o parasita depende da interação com os endossomas tardios e anfisomas para crescer. Vesiculas de BSA, EGF e LC3, foram, também, observadas dentro do VP, sugerindo que os parasitas são capazes de internalizar material endocítico e autofágico do hospedeiro. Mais ainda, mostramos que esta interação depende da cinase PIKfyve, responsável pela conversão do fosfoinositidio-3-fosfato no fosfoinositidio-3,5-bifosfato, uma vez que inibindo esta cinase o parasita não é capaz de crescer normalmente. Finalmente, mostramos que a proteína TRPML1, uma proteína efetora do fosfoinositidio-3,5-bifosfato, e envolvida no processo de fusão das membranas dos organelos endocíticos e autofágicos, também é necessária para o crescimento do parasita. Desta forma, o nosso estudo sugere que a membrana do VP funde com vesiculas endocíticas e autofágicas tardias, de uma forma dependente do fositidio-3,5-bifosfato e do seu effetor TRPML1, permitindo a troca de material com a célula hospedeira. Concluindo, os nossos resultados evidenciam que o processo autofágico que ocorre na célula hospedeira tem um papel duplo durante a fase hepática da malaria. Enquanto numa fase inicial os hepatócitos usam o processo autofágico como forma de defesa contra o parasita, já durante a fase de replicação o VP funde com vesiculas autofágicas e endocíticas de forma a obter os nutrientes necessários ao seu desenvolvimento.--------- ABSTRACT: Malaria, which is caused by parasites of the genus Plasmodium, is the most deadly parasitic infection in humans. Although economic development and the implementation of control measures during the last century have erradicated the disease from many areas of the world, it remains a serious human health issue, particularly in developing countries. Malaria is transmitted by female mosquitoes of the genus Anopheles. During the mosquito blood meal, Plasmodium spp. sporozoites are injected into the skin dermis of the vertebrate host, followed by an obligatory liver stage. Upon entering the liver, Plasmodium parasites infect hepatocytes and silently replicate inside a host cell-derived parasitophorous vacuole (PV) into thousands of merozoites. These new parasite forms can infect red blood cells initiating the the blood stage of the disease which shows the characteristic febrile malaria episodes. The liver stage is the least characterized step of the malaria infection. Moreover, the interactions between the Plasmodium spp. PV and the host cell trafficking pathways are poorly understood. We dissected the interaction between Plasmodium parasites and the host cell endocytic and autophagic pathways and we found that both pathways intersect and interconnect in the close vicinity of the parasite PV, where amphisomes are formed and accumulate. Interestingly, we observed a clearance function for autophagy in hepatocytes infected with Plasmodium berghei parasites at early infection times, whereas during late liver stage development late endosomes and amphisomes are required for parasite growth. Moreover, we found the presence of internalized BSA, EGF and LC3 inside parasite vacuoles, suggesting that the parasites uptake endocytic and autophagic cargo. Furthermore, we showed that the interaction between the PV and host traffic pathways is dependent on the kinase PIKfyve, which converts the phosphoinositide PI(3)P into PI(3,5)P2, since PIKfyve inhibition caused a reduction in parasite growth. Finally, we showed that the PI(3,5)P2 effector protein TRPML1, which is involved in late endocytic and autophagic membrane fusion, is also required for parasite development. Thus, our studies suggest that the parasite parasitophorous vacuole membrane (PVM) is able to fuse with late endocytic and autophagic vesicles in a PI(3,5)P2- and TRPML1-dependent manner, allowing the exchange of material between the host cell and the parasites, necessary for the rapid development of the latter that is seen during the liver stage of infection. In conclusion, we present evidence supporting a specific and essential dual role of host autophagy during the course of Plasmodium liver infection. Whereas in the initial hours of infection the host cell uses autophagy as a cell survival mechanism to fight the infection, during the replicative phase the PV fuses with host autophagic and endocytic vesicles to obtain nutrients required for parasite growth.

Toxocariasis of the central nervous system: with report of two cases

Clinical involvement of the nervous system in visceral larva migrans due to Toxocara is rare, although in experimental animals the larvae frequently migrate to the brain. A review of the literature from the early 50's to date found 29 cases of brain involvement in toxocariasis. In 20 cases, various clinical and laboratory manifestations of eosinophilic meningitis, encephalitis, myelitis or radiculopathy were reported. We report two children with neurological manifestations, in which there was cerebrospinal fluid pleocytosis with marked eosinophilia and a positive serology for Toxocara both in serum and CSF. Serology for Schistosoma mansoni, Cysticercus cellulosae, Toxoplasma and cytomegalovirus were negative in CSF, that was sterile in both cases. Improvement of signs and symptoms after specific treatment (albendazole or thiabendazole) was observed in the two cases. A summary of data described in the 25 cases previously reported is presented and we conclude that in cases of encephalitis and myelitis with cerebrospinal fluid pleocytosis and eosinophilia, parasitic infection of the central nervous system should be suspected and serology should be performed to establish the correct diagnosis and treatment.

Prevalence of Mansonella ozzardi among riverine communities in the municipality of Lábrea, State of Amazonas, Brazil

INTRODUCTION: Estimate the prevalence of Mansonella ozzardi infection and calculate the parasitic infection rate (PIR) in simuliid black flies in the municipality of Lábrea, State of Amazonas, Brazil. METHODS: Prevalence was measured using the thick blood smear method collected from the fingers and was related to age, sex and occupation. Simuliidae were collected with a suction apparatus, then stained with hematoxylin and dissected to verify the PIR. RESULTS: The average prevalence rate of M. ozzardi among the 694 individuals examined was 20.7%. Infection was higher in men (27.6%) than in women (14.3%) (p < 0.001) and occurred in most age groups, with the highest prevalence in the following age groups: 38-47 (40%), 48-57 (53.1%) and >58 (60.5%). The highest prevalence rates were observed in the retired (64%), followed by farm workers (47.1%). Infection by M. ozzardi was only identified in Cerqueirellum amazonicum (Simuliidae) with a PIR of 0.6%. CONCLUSIONS: This study showed a high prevalence of M. ozzardi in the riverine communities of Lábrea due to the lack of policies regarding the treatment of microfilaremic individuals in the region and an abundance of competent vectors for M. ozzardi.

Chagas disease in the State of Amazonas: history, epidemiological evolution, risks of endemicity and future perspectives

Chagas disease (CD) is a parasitic infection that originated in the Americas and is caused by Trypanosoma cruzi. In the last few years, the disease has spread to countries in North America, Asia and Europe due to the migration of Latin Americans. In the Brazilian Amazon, CD has an endemic transmission, especially in the Rio Negro region, where an occupational hazard was described for piaçaveiros (piassaba gatherers). In the State of Amazonas, the first chagasic infection was reported in 1977, and the first acute CD case was recorded in 1980. After initiatives to integrate acute CD diagnostics with the malaria laboratories network, reports of acute CD cases have increased. Most of these cases are associated with oral transmission by the consumption of contaminated food. Chronic cases have also been diagnosed, mostly in the indeterminate form. These cases were detected by serological surveys in cardiologic outpatient clinics and during blood donor screening. Considering that the control mechanisms adopted in Brazil's classic transmission areas are not fully applicable in the Amazon, it is important to understand the disease behavior in this region, both in the acute and chronic cases. Therefore, the pursuit of control measures for the Amazon region should be a priority given that CD represents a challenge to preserving the way of life of the Amazon's inhabitants.

Seasonality, parity rates and transmission indices of Mansonella ozzardi (Manson) (Nematoda: Onchocercidae) by Cerqueirellum argentiscutum (Shelley & Luna Dias) (Diptera: Simulidae) in a lower Solimões River community, Amazonas, Brazil

Mansonella ozzardi is transmitted by two dipterian families, Ceratopogonidae (midges) and Simuliidae (black flies). In Brazil, black flies are vectors for this filariasis until now. In this paper, we determined the seasonality, parity capacity and parasitic infection rate of Cerqueirellum argentiscutum. The work was carried out in the Porto Japão community, Lower Solimões River, Amazonas, Brazil. Results show that the black flies were more abundant during the rainy season (from December to May). The number of parous flies was higher in every sampling during the course of year. Monthly Biting Rate (MBR1 123742.00, MBR2 86701.50) was high, although Parasitic Infection Rate (PIR1 0.06, PIR2 0.08) and Annual Transmission Potential (ATP 7.25) were low in numbers.

Epidemiological studies of Mansonella ozzardi (Nematoda, Onchocercidae) in indigenous communities of Pauini municipality, Amazonas, Brazil

The Mansonella ozzardi has a widespread distribution among the indigenous and riverine communities of Amazonas, Brazil. We estimated the prevalence of Mansonella ozzardi in indigenous communities of the Pauini municipality, Amazonas state, Brazil and the rate of parasitic infection in vectors. We collected thick blood smears from individuals from six Apurinã indigenous communities along the Purus River and its tributaries. Collections of simuliids were made and dissected, and the larval instars of M. ozzardi identified. The overall prevalence of M. ozzardi was 28.40%, with the highest incidence among males and agricultural workers. Among age groups, children 2-9 years of age had the lowest incidence, while individuals older than 58 exhibited the highest rates of infection. We found infected simuliids in three communities, with Parasitic Infection Rates (PIR) of 0.34-6.58%. The prevalence of M. ozzardi among the Apurinã people is high, possibly related to the diary activities of the riparian people, where a high abundance of the vectors exists.

The pro-allergic influences of helminth parasites

Parasitic infection is highly allergenic, and the present paper illustrates how parasites might disrupt the regulation of IgE synthesis, resulting in heightened Th-2 responses. The study of parasites, and dysregulation of the IgE ntwork, could in turn provide information relating to the aetiology of allergic diseases such as asthma and atopic dermatitis.

IL-5 and IL-5 receptor in asthma

Eosinophils, along with mast cells are key cells involved in the innate immune response against parasitic infection whereas the adaptive immune response is largely dependent on lymphocytes. In chronic parasitic disease and in chronic allergic disease, IL-5 is predominantly a T cell derived cytokine which is particularly important for the terminal differentiation, activation and survival of committed eosinophil precursors. The human IL-5 gene is located on chromosome 5 in a gene cluster that contains the evolutionary related IL-4 family of cytokine genes. The human IL-5 receptor complex is a heterodimer consisting of a unique a subunit (predominantly expressed on eosinophils) and a beta subunit which is shared between the receptors for IL-3 & GM-CSF (more widely expressed). The a subunit is required for ligand-specific binding whereas association with the beta subunit results in increased binding affinity. The alternative splicing of the alphaIL-5R gene which contains 14 exons can yield several alphaIL-5R isoforms including a membrane-anchored isoform (alphaIL-5Rm) and a soluble isoform (alphaIL-5Rs). Cytokines such as IL-5 produce specific and non-specific cellular responses through specific cell membrane receptor mediated activation of intracellular signal transduction pathways which, to a large part, regulate gene expression. The major intracellular signal transduction mechanism is activation of non-receptor associated tyrosine kinases including JAK and MAP kinases which can then transduce signals via a novel family of transcriptional factors named signal transducers and activators of transcription (STATS). JAK2, STAT1 and STAT 5 appear to be particularly important in IL-5 mediated eosinophil responses. Asthma is characterized by episodic airways obstruction, increased bronchial responsiveness, and airway inflammation. Several studies have shown an association between the number of activated T cells and eosinophils in the airways and abnormalities in FEV1, airway reactivity and clinical severity in asthma. It has now been well documented that IL-5 is highly expressed in the bronchial mucosa of atopic and intrinsic asthmatics and that the increased IL-5 mRNA present in airway tissues is predominantly T cell derived. Immunocytochemical staining of bronchial biopsy sections has confirmed that IL-5 mRNA transcripts are translated into protein in asthmatic subjects. Furthermore, the number of activated CD 4 + T cells and IL-5 mRNA positive cells are increased in asthmatic airways following antigen challenge and studies that have examined IL-5 expression in asthmatic subjects before and after steroids have shown significantly decreased expression following oral corticosteroid treatment in steroid-sensitive asthma but not in steroid resistant and chronic severe steroid dependent asthma. The link between T cell derived IL-5 and eosinophil activation in asthmatic airways is further strengthened by the demonstration that there is an increased number of alphaIL-5R mRNA positive cells in the bronchial biopsies of atopic and non-atopic asthmatic subjects and that the eosinophil is the predominant site of this increased alphaIL-5R mRNA expression. We have also shown that the subset of activated eosinophils that expressed mRNA for membrane bound alpha IL5r inversely correlated with FEV1, whereas the subset of activated eosinophils that expressed mRNA for soluble alphaIL5r directly correlated with FEV1. Hence, not only does this data suggest that the presence of eosinophils expressing alphaIL-5R mRNA contribute towards the pathogenesis of bronchial asthma, but also that the eosinophil phenotype with respect to alphaIL-5R isoform expression is of central importance. Finally, there are several animal, and more recently in vitro lung explant, models of allergen induced eosinophilia, late airway responses(LARS), and bronchial hyperresponsiveness(BHR) - all of which support a link between IL-5 and airway eosinophila and bronchial hyperresponsiveness. The most direct demonstration of T cell involvement in LARS is the finding that these physiological responses can be transferred by CD4+ but not CD8+ T cells in rats. The importance of IL-5 in animal models of allergen induced bronchial hyperresponsiveness has been further demonstrated by a number of studies which have indicated that IL-5 administration is able to induce late phase responses and BHR and that anti-IL-5 antibody can block allergen induced late phase responses and BHR. In summary, activated T lymphocytes, IL5 production and eosinophil activation are particularly important in the asthmatic response. Human studies in asthma and studies in allergic animal models have clearly emphasised the unique role of IL-5 in linking T lymphocytes and adaptive immunity, the eosinophil effector cell, and the asthma phenotype. The central role of activated lymphocytes and eosinophils in asthma would argue for the likely therapeutic success of strategies to block T cell and eosinophil activation (eg steroids). Importantly, more targeted therapies may avoid the complications associated with steroids. Such therapies could target key T cell activation proteins and cytokines by various means including blocking antibodies (eg anti-CD4, anti-CD40, anti-IL-5 etc), antisense oligonucleotides to their specific mRNAs, and/or selective inhibition of the promoter sites for these genes. Another option would be to target key eosinophil activation mechanisms including the aIL5r. As always, the risk to benefit ratio of such strategies await the results of well conducted clinical trials.

TREM-1 deficiency can attenuate disease severity without affecting pathogen clearance.

Triggering receptor expressed on myeloid cells-1 (TREM-1) is a potent amplifier of pro-inflammatory innate immune reactions. While TREM-1-amplified responses likely aid an improved detection and elimination of pathogens, excessive production of cytokines and oxygen radicals can also severely harm the host. Studies addressing the pathogenic role of TREM-1 during endotoxin-induced shock or microbial sepsis have so far mostly relied on the administration of TREM-1 fusion proteins or peptides representing part of the extracellular domain of TREM-1. However, binding of these agents to the yet unidentified TREM-1 ligand could also impact signaling through alternative receptors. More importantly, controversial results have been obtained regarding the requirement of TREM-1 for microbial control. To unambiguously investigate the role of TREM-1 in homeostasis and disease, we have generated mice deficient in Trem1. Trem1(-/-) mice are viable, fertile and show no altered hematopoietic compartment. In CD4(+) T cell- and dextran sodium sulfate-induced models of colitis, Trem1(-/-) mice displayed significantly attenuated disease that was associated with reduced inflammatory infiltrates and diminished expression of pro-inflammatory cytokines. Trem1(-/-) mice also exhibited reduced neutrophilic infiltration and decreased lesion size upon infection with Leishmania major. Furthermore, reduced morbidity was observed for influenza virus-infected Trem1(-/-) mice. Importantly, while immune-associated pathologies were significantly reduced, Trem1(-/-) mice were equally capable of controlling infections with L. major, influenza virus, but also Legionella pneumophila as Trem1(+/+) controls. Our results not only demonstrate an unanticipated pathogenic impact of TREM-1 during a viral and parasitic infection, but also indicate that therapeutic blocking of TREM-1 in distinct inflammatory disorders holds considerable promise by blunting excessive inflammation while preserving the capacity for microbial control.