Worm Expulsion Research Articles

Functions of Group 2 Innate Lymphoid Cells in Tumor Microenvironment.

Innate lymphoid cells (ILCs), defined as a heterogeneous population of lymphocytes, have received much attention over recent years. They can be categorized into three subsets according to the expression profiles of transcription factors and differing levels of cytokine production. These cells are widely distributed in human organs and tissues, especially in mucosal tissue. The ILCs are involved in various physiological and pathological processes, including inflammation, worm expulsion, autoimmune disease and tumor progression, many of which have been investigated and clarified in recent studies. In the tumor microenvironment, group 2 innate lymphoid cells (ILC2s) have been proved to be able to either promote or inhibit tumor progression by producing different cytokines, recruiting diverse types of immune cells, expressing immunosuppressive molecules and by regulating the expression of certain inflammatory factors. This review summarizes recent research progress on the immunomodulatory functions of ILC2s in the tumor microenvironment and puts forward some perspectives for future study.

TGFβ-activation by dendritic cells drives Th17 induction and intestinal contractility and augments the expulsion of the parasite Trichinella spiralis in mice.

Helminths are highly prevalent metazoan parasites that infect over a billion of the world’s population. Hosts have evolved numerous mechanisms to drive the expulsion of these parasites via Th2-driven immunity, but these responses must be tightly controlled to prevent equally devastating immunopathology. However, mechanisms that regulate this balance are still unclear. Here we show that the vigorous Th2 immune response driven by the small intestinal helminth Trichinella spiralis, is associated with increased TGFβ signalling responses in CD4+ T-cells. Mechanistically, enhanced TGFβ signalling in CD4+ T-cells is dependent on dendritic cell-mediated TGFβ activation which requires expression of the integrin αvβ8. Importantly, mice lacking integrin αvβ8 on DCs had a delayed ability to expel a T. spiralis infection, indicating an important functional role for integrin αvβ8-mediated TGFβ activation in promoting parasite expulsion. In addition to maintaining regulatory T-cell responses, the CD4+ T-cell signalling of this pleiotropic cytokine induces a Th17 response which is crucial in promoting the intestinal muscle hypercontractility that drives worm expulsion. Collectively, these results provide novel insights into intestinal helminth expulsion beyond that of classical Th2 driven immunity, and highlight the importance of IL-17 in intestinal contraction which may aid therapeutics to numerous diseases of the intestine.

Parasitic nematodes simultaneously suppress and benefit from coccidian coinfection in their natural mouse host.

Within-host interactions among coinfecting parasites are common and have important consequences for host health and disease dynamics. However, these within-host interactions have traditionally been studied in laboratory mouse models, which often exclude important variation and use unnatural host-parasite combinations. Conversely, the few wild studies of within-host interactions often lack knowledge of parasite exposure and infection history. Here we exposed laboratory-reared wood mice (Apodemus sylvaticus) that were derived from wild-caught animals to two naturally-occurring parasites (nematode: Heligmosomoides polygyrus, coccidia: Eimeria hungaryensis) to investigate the impact of coinfection on parasite infection dynamics, and to determine if the host immune response mediates this interaction. Coinfection led to delayed worm expulsion and prolonged egg shedding in H. polygyrus infections and lower peak E. hungaryensis oocyst burdens. By comparing antibody levels between wild and colony-housed mice, we also found that wild mice had elevated H. polygyrus-IgG1 titres even if currently uninfected with H. polygyrus. Using this unique wild-laboratory system, we demonstrate, for the first time, clear evidence for a reciprocal interaction between these intestinal parasites, and that there is a great discrepancy between antibody levels measured in the wild vs those measured under controlled laboratory conditions in relation to parasite infection and coinfection.

Role of mast cells in the generation of a T-helper type 2 dominated anti-helminthic immune response.

Mast cells are long-lived, innate immune cells of the myeloid lineage which are found in peripheral tissues located throughout the body, and positioned at the interface between the host and the environment. Mast cells are found in high concentrations during helminth infection. Using Kitw-sh mast cell deficient mice, a recently published study in Bioscience Reports by Gonzalez et al. (Biosci. Rep., 2018) focused on the role of mast cells in the immune response to infection by the helminth Hymenolepis diminuta. The authors showed that mast cells play a role in the modulation of Th2 immune response characterized by a unique IL-4, IL-5 and IL-13 cytokine profile, as well as subsequent robust worm expulsion during H. diminuta infection. Unlike WT mice which expelled H. diminuta at day 10, Kitw-sh deficient mice displayed delayed worm expulsion (day 14 post infection). Further, a possible role for mast cells in the basal expression of cytokines IL-25, IL-33 and thymic stromal lymphopoietin was described. Deletion of neutrophils in Kitw-sh deficient mice enhanced H. diminuta expulsion, which was accompanied by splenomegaly. However, interactions between mast cells and other innate and adaptive immune cells during helminth infections are yet to be fully clarified. We conclude that the elucidation of mechanisms underlying mast cell interactions with cells of the innate and adaptive immune system during infection by helminths can potentially uncover novel therapeutic applications against inflammatory, autoimmune and neoplastic diseases.

Exclusive dependence of IL-10Rα signalling on intestinal microbiota homeostasis and control of whipworm infection.

The whipworm Trichuris trichiura is a soil-transmitted helminth that dwells in the epithelium of the caecum and proximal colon of their hosts causing the human disease, trichuriasis. Trichuriasis is characterized by colitis attributed to the inflammatory response elicited by the parasite while tunnelling through intestinal epithelial cells (IECs). The IL-10 family of receptors, comprising combinations of subunits IL-10Rα, IL-10Rβ, IL-22Rα and IL-28Rα, modulates intestinal inflammatory responses. Here we carefully dissected the role of these subunits in the resistance of mice to infection with T. muris, a mouse model of the human whipworm T. trichiura. Our findings demonstrate that whilst IL-22Rα and IL-28Rα are dispensable in the host response to whipworms, IL-10 signalling through IL-10Rα and IL-10Rβ is essential to control caecal pathology, worm expulsion and survival during T. muris infections. We show that deficiency of IL-10, IL-10Rα and IL-10Rβ results in dysbiosis of the caecal microbiota characterised by expanded populations of opportunistic bacteria of the families Enterococcaceae and Enterobacteriaceae. Moreover, breakdown of the epithelial barrier after whipworm infection in IL-10, IL-10Rα and IL-10Rβ-deficient mice, allows the translocation of these opportunistic pathogens or their excretory products to the liver causing organ failure and lethal disease. Importantly, bone marrow chimera experiments indicate that signalling through IL-10Rα and IL-10Rβ in haematopoietic cells, but not IECs, is crucial to control worm expulsion and immunopathology. These findings are supported by worm expulsion upon infection of conditional mutant mice for the IL-10Rα on IECs. Our findings emphasize the pivotal and complex role of systemic IL-10Rα signalling on immune cells in promoting microbiota homeostasis and maintaining the intestinal epithelial barrier, thus preventing immunopathology during whipworm infections.

Mast cell deficiency in mice results in biomass overgrowth and delayed expulsion of the rat tapeworm Hymenolepis diminuta.

Infection with helminth parasites evokes a complex cellular response in the host, where granulocytes (i.e. eosinophils, basophils and mast cells (MCs)) feature prominently. In addition to being used as markers of helminthic infections, MCs have been implicated in worm expulsion since animals defective in c-kit signaling, which results in diminished MC numbers, can have delayed worm expulsion. The role of MCs in the rejection of the rat tapeworm, Hymenolepsis diminuta, from the non-permissive mouse host is not known. MC-deficient mice display a delay in the expulsion of H. diminuta that is accompanied by a less intense splenic Th2 response, as determined by in vitro release of interleukin (IL)-4, IL-5 and IL-13 cytokines. Moreover, worms retrieved from MC-deficient mice were larger than those from wild-type (WT) mice. Assessment of gut-derived IL-25, IL-33, thymic stromal lymphopoietin revealed lower levels in uninfected MC-deficient mice compared with WT, suggesting a role for MCs in homeostatic control of these cytokines: differences in these gut cytokines between the mouse strains were not observed after infection with H. diminuta. Finally, mice infected with H. diminuta display less severe dinitrobenzene sulphonic acid (DNBS)-induced colitis, and this beneficial effect of the worm was unaltered in MC-deficient mice challenged with DNBS, as assessed by a macroscopic disease score. Thus, while MCs are not essential for rejection of H. diminuta from mice, their absence slows the kinetics of expulsion allowing the development of greater worm biomass prior to successful rejection of the parasitic burden.

Co-expulsion of Ascaridia galli and Heterakis gallinarum by chickens

Worm expulsion is known to occur in mammalian hosts exposed to mono-species helminth infections, whilst this phenomenon is poorly described in avian hosts. Mono-species infections, however, are rather rare under natural circumstances. Therefore, we quantified the extent and duration of worm expulsion by chickens experimentally infected with both Ascaridia galli and Heterakis gallinarum, and investigated the accompanying humoral and cell-mediated host immune responses in association with population dynamics of the worms. Results demonstrated the strong co-expulsion of the two ascarid species in three phases. The expulsion patterns were characterized by non-linear alterations separated by species-specific time thresholds. Ascaridia galli burden decreased at a daily expulsion rate (e) of 4.3 worms up to a threshold of 30.5 days p.i., followed by a much lower second expulsion rate (e = 0.46), which resulted in almost, but not entirely, complete expulsion. Heterakis gallinarum was able to induce reinfection within the experimental period (9 weeks). First generation H. gallinarum worms were expelled at a daily rate of e = 0.8 worms until 36.4 days p.i., and thereafter almost no expulsion occurred. Data on both humoral and tissue-specific cellular immune responses collectively indicated that antibody production in chickens with multispecies ascarid infections is triggered by Th2 polarisation. Local Th2 immune responses and mucin-regulating genes are associated with the regulation of worm expulsion. In conclusion, the chicken host is able to eliminate the vast majority of both A. galli and H. gallinarum in three distinct phases. Worm expulsion was strongly associated with the developmental stages of the worms, where the elimination of juvenile stages was specifically targeted. A very small percentage of worms was nevertheless able to survive, reach maturity and induce reinfection if given sufficient time to complete their life cycle. Both humoral and local immune responses were associated with worm expulsion.

Worm expulsion of Gymnophalloides seoi from C57BL/6 mice: role of metacercarial exosomes in upregulating TLR2 and MUC2 expression in intestinal tissues.

Gymnophalloides seoi worms were rapidly expelled from C57BL/6 mice within days 3-6 post-infection probably due to operation of mucosal innate immunity. To understand better the mucosal immunity related to worm expulsion from the host, we isolated exosomes of G. seoi metacercariae and investigated their role in induction of mRNA and protein expression of several Toll-like receptors and mucin-related factors in vitro. G. seoi-secreted exosomes were collected using differential ultracentrifugation, and cellular internalization of the exosomes into HT-29 intestinal epithelial cells was visualized by confocal microscopy. The expression of TLR2 and MUC2 in HT-29 cells was up-regulated in stimulation with the exosomes. We suggest that G. seoi-secreted exosomes offer a new point of view in the mechanism of worm expulsion from the host through enhancement of TLR2 and MUC2 expression.

Comment on “The optimal timing of post-treatment sampling for the assessment of anthelminthic drug efficacy against Ascaris infections in humans”

A recent publication by Levecke et al. (Int. J. Parasitol, 2018, 8, 67–69) provides important insights into the kinetics of worm expulsion from humans following treatment with albendazole. This is an important aspect of determining the optimal time-point for post treatment sampling to examine anthelmintic drug efficacy. The authors conclude that for the determination of drug efficacy against Ascaris, samples should be taken not before day 14 and recommend a period between days 14 and 21. Using this recommendation, they conclude that previous data (Krücken et al., 2017; Int. J. Parasitol, 7, 262–271) showing a reduction of egg shedding by 75.4% in schoolchildren in Rwanda and our conclusions from these data should be interpreted with caution. In reply to this, we would like to indicate that the very low efficacy of 0% in one school and 52–56% in three other schools, while the drug was fully efficient in other schools, cannot simply be explained by the time point of sampling. Moreover, there was no correlation between the sampling day and albendazole efficacy. We would also like to indicate that we very carefully interpreted our data and, for example, nowhere claimed that we found anthelmintic resistance. Rather, we stated that our data indicated that benzimidazole resistance may be suspected in the study population. We strongly agree that the data presented by Levecke et al. suggests that recommendations for efficacy testing of anthelmintic drugs should be revised.

A2B Adenosine Receptor Signaling on Epithelial Cells Promotes Type 2 Immunity Against Helminths

Abstract Intestinal helminth infections trigger potent type 2 immune responses, although the mechanisms that initiate these host protective responses against these multicellular parasites remain uncertain. We have previously reported that inoculation with the murine intestinal nematode parasite Heligmosomoides polygyrus (Hp) results in rapid increases in intestinal epithelial surface expression of the ectonucleotidases, CD39 and CD73, which in turn degrade extracellular ATP into adenosine. Adenosine binds to adenosine G-protein-coupled cell surface receptors (A1, A2A, A2B and A3 –AR). Mice deficient in A2BAR have an impaired type 2 immune response and delayed worm expulsion during helminth infection. We now report that mice lacking A2BAR specifically on intestinal epithelial cells (Villin-Cre-A2BARfl/fl), but not on myeloid cells (LysMCre-A2BARfl/fl), have an impaired type 2 memory immune response with delayed worm expulsion and decreased egg production after Hp secondary inoculation. pSTAT6 levels in CD4+ T cells and B cell MHC-II surface expression (an indicator of IL-4 activity) from mesenteric lymph nodes of Villin-Cre-A2BARfl/fl mice were significantly decreased after primary Hp inoculation. Taken together, our data demonstrate a key role for epithelial cell specific A2BAR signaling in the initiation of the protective type 2 immune response to helminth infection. These studies indicate that extracellular adenosine binding to epithelial cell A2BAR acts as an endogenous danger signal that is released following helminth infection, which triggers host protective type 2 immune responses.

MicroRNAs in type 2 immunity

Type 2 immunity drives the pathology of allergic diseases and is necessary for expulsion of parasitic worms as well as having important implications in tumor progression. Over the last decade, a new research field has emerged describing a significant link between type 2 immunity and cancer development, called AllergoOncology. Thus, type 2 immune responses must be carefully regulated to mediate effective protection against damaging environmental factors, yet avoid excessive activation and immunopathology. Regulation of gene expression by microRNAs is required for normal behavior of most mammalian cells and has been studied extensively in the context of cancer. Although microRNA regulation of the immune system in cancer is well established and includes type 2 immune reactions in the tumor microenvironment, the involvement of microRNAs in these responses initiated by allergens, parasites or other environmental factors is just emerging. In this review, we focus on recent advances which increase the understanding of microRNA-mediated regulation of key mechanisms of type 2 immunity.

The circadian regulator BMAL1 programmes responses to parasitic worm infection via a dendritic cell clock

Resistance to the intestinal parasitic helminth Trichuris muris requires T-helper 2 (TH2) cellular and associated IgG1 responses, with expulsion typically taking up to 4 weeks in mice. Here, we show that the time-of-day of the initial infection affects efficiency of worm expulsion, with strong TH2 bias and early expulsion in morning-infected mice. Conversely, mice infected at the start of the night show delayed resistance to infection, and this is associated with feeding-driven metabolic cues, such that feeding restriction to the day-time in normally nocturnal-feeding mice disrupts parasitic expulsion kinetics. We deleted the circadian regulator BMAL1 in antigen-presenting dendritic cells (DCs) in vivo and found a loss of time-of-day dependency of helminth expulsion. RNAseq analyses revealed that IL-12 responses to worm antigen by circadian-synchronised DCs were dependent on BMAL1. Therefore, we find that circadian machinery in DCs contributes to the TH1/TH2 balance, and that environmental, or genetic perturbation of the DC clock results in altered parasite expulsion kinetics.

Intestinal immunity suppresses carrying capacity of rats for the model tapeworm, Hymenolepis diminuta

Hymenolepis diminuta is a parasitic tapeworm of the rat small intestine and is recognized as a useful model for the analysis of cestode-host interactions. In this study, we analyzed factors affecting the biomass of the tapeworm through use of rat strains carrying genetic mutations, namely X-linked severe combined immunodeficiency (xscid; T, B and NK cells deficiency), nude (rnu; T cell deficiency), and mast cell deficient rats. The worm biomass of F344-xscid rats after infection with 5 cysticercoids was much larger than control F344 rats from 3 to 8 weeks. The biomass of F344-rnu rats was also larger than the controls, but was intermediate between F344-xscid and control rats. These observations demonstrated that host immunity can control the maximal tapeworm biomass, i.e., carrying capacity, of the rat small intestine. Both T cell and other immune cells (B and NK cells) have roles in determining the carrying capacity of tapeworms. Total worm biomass and worm numbers in mast cell deficient rats (WsRC-Ws/Ws) were not significantly different from control WsRC-+/+ rats after 3 and 6 weeks of primary infection. Mast cell deficient rats displayed reinfection resistance for worm biomass but not worm expulsion. These findings suggest that the mast cell has a role for controlling the biomass of this tapeworm in reinfection alone, but does not affect the rate of worm expulsion. Overall, our findings indicate that the mast cell is not a major effector cell for the control of the carrying capacity of tapeworms. The identity of the major effector cell remains unknown.

The optimal timing of post-treatment sampling for the assessment of anthelminthic drug efficacy against Ascaris infections in humans

The egg reduction rate (ERR) is the current standard mean to assess the efficacy of drugs against human soil-transmitted helminths (STHs; Ascaris lumbricoides, Trichuris trichiura and hookworm). Although the timing of post-treatment sampling is pivotal for a readily interpretation of drug efficacy, there is lack empirical data that allows recommending the optimal time point for a follow-up egg counting. In the present study, we re-analyzed both the kinetics of worm expulsion and egg output for Ascaris lumbricoides following a single oral dose of albendazole in a series of studies previously conducted in Kenyan communities. The results indicate that it takes up to 10 days post-treatment before the expulsion of both adult male and female Ascaris worms is completed, approximately 20% of the worms being expelled between day 7 and 10 post-treatment. The sequential analysis of the egg out put, indicated a poor ERR (89.4%) at day 7 post-treatment, but a 100% ERR at day 14 and 21 post-treatment. Based on our findings we recommend to wait at least 14 days after an albendazole treatment before conducting the follow-up egg count. Any sampling before this time point may result in biased ERR estimates, due the release of residual eggs from moribund or degenerating worms.

Histopathological changes in the liver and stomach of Didelphis virginiana (Didelphimorphia: Didelphidae) during natural infection with Gnathostoma turgidum (Nematoda: Gnathostomidae).

Gnathostoma turgidum is a nematode parasite that exploits the stomach of Virginian opossums, Didelphis virginiana, in Latin America. The opossum is the definitive host of G. turgidum in the wild. Intrahepatic growth and maturation of the parasite, subsequent migration to the stomach and spontaneous expulsion are common. However, the histopathological lesions caused by G. turgidum are poorly described. A better understanding of the life cycle of this parasite and the pathological changes in natural host-parasite interactions could help to clarify the progression of human infections caused by Gnathostoma binucleatum. The aim of this work was to study morphological changes in the liver and stomach of D. virginiana during natural infection and adult worm expulsion. Three opossums naturally infected with G. turgidum were captured from an endemic area of gnathostomosis. Three uninfected opossums captured from a non-endemic area were used as controls. The opossums were sacrificed at different stages of infection (March, May and December), and a histopathological study of their livers and stomachs was conducted. Injuries in livers were observed by histopathology - areas of necrosis and collagen septa were identified. Parasites caused nodules with necrosis on the periphery of lesions, and collagen fibres were also observed in stomachs. Collagen septa may be caused by antigenic remains of the parasite. Further immunological studies are necessary to verify that stimulation is caused by these factors.

ILC2s activated by IL-25 promote antigen-specific Th2 and Th9 functions that contribute to the control of Trichinella spiralis infection.

IL-25, an IL-17 family cytokine, derived from epithelial cells was shown to regulate Th2- and Th9-type immune responses. We previously reported that IL-25 was important in promoting efficient protective immunity against T. spiralis infection; however, the cellular targets of IL-25 to elicit type-2 immunity during infection have not yet been addressed. Here, we investigated IL-25-responding cells and their involvement in mediating type-2 immune response during T. spiralis infection. ILC2 and CD4+ Th2 cells residing in the gastrointestinal tract of T. spiralis infected mice were found to express high levels of surface interleukin-17 receptor B (IL-17RB), a component of the IL-25 receptor. Following T. spiralis infection, activated ILC2s upregulated surface MHCII expression and enhanced capacity of effector T helper cell in producing antigen-specific Th2 and Th9 cytokines through MHCII-dependent interactions. Reciprocally, lack of CD4+ T helper cells impaired ILC2 function to produce type 2-associated cytokines in responding to IL-25 during T. spiralis infection. Furthermore, mice deficient in IL-17RB showed markedly reduced ILC2 numbers and antigen-specific Th2 and Th9 cytokine production during T. spiralis infection. The Il17rb-/- mice failed to mount effective antigen specific Th2 and Th9 functions resulting in diminished goblet cell and mast cell responses, leading to delayed worm expulsion in the intestines and muscles. Thus, our data indicated that ILC2s and CD4+ Th2 cells are the predominant cellular targets of IL-25 following T. spiralis infection and their collaborative interactions may play a key role in mounting effective antigen-specific Th2 and Th9 cytokine responses against T. spiralis infection.

TPL-2 restricts Ccl24-dependent immunity to Heligmosomoides polygyrus.

TPL-2 (COT, MAP3K8) kinase activates the MEK1/2-ERK1/2 MAPK signaling pathway in innate immune responses following TLR, TNFR1 and IL-1R stimulation. TPL-2 contributes to type-1/Th17-mediated autoimmunity and control of intracellular pathogens. We recently demonstrated TPL-2 reduces severe airway allergy to house dust mite by negatively regulating type-2 responses. In the present study, we found that TPL-2 deficiency resulted in resistance to Heligmosomoides polygyrus infection, with accelerated worm expulsion, reduced fecal egg burden and reduced worm fitness. Using co-housing experiments, we found resistance to infection in TPL-2 deficient mice (Map3k8–/–) was independent of microbiota alterations in H. polygyrus infected WT and Map3k8–/–mice. Additionally, our data demonstrated immunity to H. polygyrus infection in TPL-2 deficient mice was not due to dysregulated type-2 immune responses. Genome-wide analysis of intestinal tissue from infected TPL-2-deficient mice identified elevated expression of genes involved in chemotaxis and homing of leukocytes and cells, including Ccl24 and alternatively activated genes. Indeed, Map3k8–/–mice had a significant influx of eosinophils, neutrophils, monocytes and Il4GFP+ T cells. Conditional knockout experiments demonstrated that specific deletion of TPL-2 in CD11c+ cells, but not Villin+ epithelial cells, LysM+ myeloid cells or CD4+ T cells, led to accelerated resistance to H. polygyrus. In line with a central role of CD11c+ cells, CD11c+ CD11b+ cells isolated from TPL-2-deficient mice had elevated Ccl24. Finally, Ccl24 neutralization in TPL-2 deficient mice significantly decreased the expression of Arg1, Retnla, Chil3 and Ear11 correlating with a loss of resistance to H. polygyrus. These observations suggest that TPL-2-regulated Ccl24 in CD11c+CD11b+ cells prevents accelerated type-2 mediated immunity to H. polygyrus. Collectively, this study identifies a previously unappreciated role for TPL-2 controlling immune responses to H. polygyrus infection by restricting Ccl24 production.

ILC2s regulate adaptive Th2 cell functions via PD-L1 checkpoint control.

Group 2 innate lymphoid cells (ILC2s) are important effector cells driving the initiation of type 2 immune responses leading to adaptive T helper 2 (Th2) immunity. Here we show that ILC2s dynamically express the checkpoint inhibitor molecule PD-L1 during type 2 pulmonary responses. Surprisingly, PD-L1:PD-1 interaction between ILC2s and CD4+ T cells did not inhibit the T cell response, but PD-L1-expressing ILC2s stimulated increased expression of GATA3 and production of IL-13 by Th2 cells both in vitro and in vivo. Conditional deletion of PD-L1 on ILC2s impaired early Th2 polarization and cytokine production, leading to delayed worm expulsion during infection with the gastrointestinal helminth Nippostrongylus brasiliensis Our results identify a novel PD-L1-controlled mechanism for type 2 polarization, with ILC2s mediating an innate checkpoint to control adaptive T helper responses, which has important implications for the treatment of type 2 inflammation.

Nutritional status and its correlates in under five children of labour population in urban slums of Lucknow, Uttar Pradesh, India

Background: Malnutrition has a long-term effect on physical and cognitive development of a child. Addressing nutritional problems of urban poor living in slums is of paramount importance for overall development. Effective measures could be taken if we know their sociodemographic profile, burden of malnutrition and infant feeding practices.Methods: A prospective cross sectional study was conducted in under five children living in urban slums of Lucknow around Era’s Lucknow Medical College and Hospital after taking consent from the parents and approval by institute’s ethical committee. The objective of the study was to know the prevalence of malnutrition and assess the feeding practices, immunization status and morbidities in under five children of labour population in urban slums of Lucknow.Results: 250 children aged 6 months to 5 years were analysed. 34.4%were underweight, 58.8% stunted and 17.6%. Wasted 17.6% infants were exclusively breast fed till 6 months 42.0% fed colostrum. 20.0% children received proper complementary feeding. Education status of mother was significantly associated with the prevalence of underweight children. (p <0.05) Late initiation of breastfeeding in 13.2% infants was significantly associated with underweight (p value <0.05, OR (95% CI=1.58 (0.60-2.72) and stunting OR (95% CI=0.62 (0.29-1.29). 55.6% children were fully immunized and 16% unimmunized. Presence of Morbidities like ARI, diarrhea, worm expulsion, pallor and vitamin A deficiency was high.Conclusions: Burden of malnutrition and poor feeding practices, poor vaccination coverage makes children in this slum susceptible to illnesses. Prompt measures should be taken to address it.

Effects of In Vivo and In Vitro Treatment of Ascaris suum Eggs with Anthelmintic Agents on Embryonation and Infectivity for Mice.

Ascaris suum is an important intestinal nematode causing economic losses in swine. Anthelminthic treatment is used to control A. suum infections and is part of normal production practices. Treatment with anthelminthic agents results in expulsion of adult worms from the intestinal tract and ends further contamination of the environment with eggs. The present study was conducted to determine the effects of drug treatment on the embryonation of A. suum eggs collected from worms obtained from pigs treated with 4 different commercially available anthelmintics. The effects of treatment with abamectin, doramectin, ivermectin, flubendazole, or no treatment on embryonation of A. suum eggs collected from female A. suum expelled in the feces was determined. The embryonation of eggs obtained from pigs treated with abamectin, doramectin, and ivermectin was not significantly (P > 0.05) different from eggs from non-treated control pigs. In contrast, the embryonation of A. suum eggs collected from worms from pigs treated with flubendazole demonstrated inhibited development, and most eggs remained in the 1-cell stage (85.5%) and only 6.3% of eggs developed larvae. In another experiment, we examined the direct effects of doramectin and flubendazole added to solutions of A. suum eggs collected from non-treated control pigs. Egg cultures were exposed to direct in vitro treatment with 0.04-parts per million (ppm) doramectin or 1.0-ppm flubendazole for 24 hr (highest concentrations [Cmax] of drugs in serum) and then embryonation and infectivity for mice was determined. Treatment of eggs in vitro did not significantly effect (P > 0.05) larval development or oral infectivity for mice. Our study demonstrates that flubendazole fed to pigs results in inhibited embryonation of A. suum eggs. However, direct treatment of A. suum eggs in culture for 24 hr with flubendazole did not inhibit embryonation or oral infectivity of in vitro treated eggs. Anthelmintic treatment of pigs in vivo with abamectin, doramectin, and ivermectin had no significant (P > 0.05) effect on embryonation of A. suum eggs, and 24 hr treatment with doramectin in vitro had no direct effects (P > 0.05) on embryonation or oral infectivity of A. suum eggs.