The Effects of Honeysuckle (Lonicera caerulea L.) Berry Iridoid-Anthocyanin Extract on the Intestinal and Muscle Histopathology in Mice during Experimental Trichinellosis.

The aim of the study was to determine the effect of iridoid-anthocyanin extract from honeysuckle (Lonicera caerulea L.) (LC) berries on histopathological changes in the intestines and muscles during experimental trichinellosis in mice. The LC extract was administered to uninfected mice (LC group) and Trichinella-spiralis-infected mice (T+LC) orally at a dose of 2 g/kg bw, six times at 24 h intervals, from day 3 prior to infection to day 3 post-infection (dpi). Jejunum samples were collected on 5, 7, 14, and 21 dpi, and their histological assessment involved the villus height to crypt depth ratio (VH/CD), goblet cell (GC) number, and morphological changes. In the T. spiralis-infected muscles, the extent of inflammatory infiltration on the 14th and 21st dpi was assessed. LC in the infected mice restored the VH/CD ratio to control values on 14 dpi. A beneficial effect of the LC extract on the villus height was also observed 14 dpi in the LC and T+LC groups. No differences in the extent of inflammatory infiltration in the muscles between the T+LC and T groups were observed. In conclusion, the iridoid-anthocyanin extract from honeysuckle berry contributed to alleviating the symptoms of the intestinal phase of T. spiralis infection.

Immunomodulatory effects of chronic trichinellosis on Toxoplasma gondii RH virulent strain in experimental rats.

Mixed parasitic infections could affect the host immunological responses and re-design the pathogenesis of each other. The impact of Toxoplasma gondii (T. gondii) and Trichinella spiralis (T. spiralis) co-infection on the immune response remains unclear. The objective of the present study was to investigate the possible effect of chronic trichinellosis on the immune response of rats infected with T. gondii virulent RH strain. Animals were divided into four groups: group I: non-infected negative control; group II: infected with T. spiralis; group III: infected with T. gondii and group IV: infected with T. spiralis then infected with T. gondii 35 days post T. spiralis infection (co-infected group). The interaction between T. spiralis and T. gondii was evaluated by histopathological examination of liver and brain tissues, immunohistochemical expression of inducible nitric oxide synthase (iNOS), and ß-catenin in the brain tissues, and CD4+ and CD8+ T cells percentages, and tumor necrosis factor (TNF)-alpha expression in the spleen tissues. Along with, splenic interleukin (IL)-4 and IL-10 mRNA expression levels were measured 15 days post-Toxoplasma infection. Our study revealed that prior infection with T. spiralis leads to attenuation of Th1 response against T. gondii, including iNOS, TNF-α, and CD8+ T-cell response with improvement of the histopathological changes in the tissues. In conclusion, in the co-infected rats, a balanced immune response has been developed with the end result, improvement of the histopathological changes in the liver and brain.

Monocytes maintain central nervous system homeostasis following helminth-induced inflammation.

Neuroimmune interactions are crucial for regulating immunity and inflammation. Recent studies have revealed that the central nervous system (CNS) senses peripheral inflammation and responds by releasing molecules that limit immune cell activation, thereby promoting tolerance and tissue integrity. However, the extent to which this is a bidirectional process, and whether peripheral immune cells also promote tolerance mechanisms in the CNS remains poorly defined. Here we report that helminth-induced type 2 inflammation promotes monocyte responses in the brain that are required to inhibit excessive microglial activation and host death. Mechanistically, infection-induced monocytes express YM1 that is sufficient to inhibit tumor necrosis factor production from activated microglia. Importantly, neuroprotective monocytes persist in the brain, and infected mice are protected from subsequent lipopolysaccharide-induced neuroinflammation months after infection-induced inflammation has resolved. These studies demonstrate that infiltrating monocytes promote CNS homeostasis in response to inflammation in the periphery and demonstrate that a peripheral infection can alter the immunologic landscape of the host brain.

Seroprevalence of Taenia solium and Trichinella spiralis among Humans and Pigs in Ghana.

In this study, the seroprevalence of the intestinal worms Taenia solium and Trichinella spiralis in humans and pigs was assessed. A cross-sectional serological study design was performed. Blood samples were collected from 322 humans and 245 pigs used in the study. These were tested for markers of antibodies for Taenia solium and Trichinella spp. Demographic data such as sex, age, education, pig farming practices, and water source used were also obtained. An overall seroprevalence of 3.1% was recorded for Taenia solium in humans. There was also a statistical association between pig management system employed by pig farmers and seropositivity to Taenia solium (p = 0.005). Factors such as mode of waste disposal (p = 0.003) and water source used statistically correlated with Taenia solium seroprevalence among humans. For the pig samples, a Taenia solium seroprevalence of 24.9% was recorded. All the pig samples which tested positive for Taenia solium were reared on the free-ranged system. This study also recorded a seroprevalence of 0.31% for Trichinella spp. for humans and a seroprevalence of 4.5% for Trichinella spp. for pigs. Again, all the samples that showed serological evidence of Trichinella spp. among pigs came from those pigs which were raised on the free-ranged system. Proper pig management practice is a very important tool for controlling these intestinal parasites in both humans and animals. This study recommends public health education among the general public and good pig farming practices.

Galectin-Receptor Interactions Regulates Cardiac Pathology Caused by Trichinella spiralis Infection.

The parasitic nematode Trichinella spiralis causes trichinellosis, a serious food-borne parasitic zoonosis worldwide. Infection with T. spiralis may also cause myocarditis. In the present study, we used mouse models to assess the impact of blockage of galectin-receptor interactions by α-lactose on cardiac immunopathology during acute T. spiralis experimental infection. Our data demonstrated that, after T. spiralis infection, blockage of galectin-receptor interactions resulted in cardiac dysfunction detected by transthoracic conventional echocardiography, and increased serum Gal-3 level, a biomarker of myocardial damage. In addition, there were increased eosinophil number in peripheral blood, and increased eosinophil infiltration in the heart and spleen tissues accompanied with increased mRNA levels of eosinophil granule proteins (including eosinophil cationic protein (ECP) and eosinophil peroxidase (EPO)) and IL-5 in these organs; increased cardiac fibrosis accompanied with increased Gal-3 and collagen 1 expressions in the hearts of mice with blockage of galectin-receptor interactions after T. spiralis infection. Correlation analysis showed that significant positive correlations existed between the mRNA levels of Gal-3 and ECP/EPO/eosinophil major basic protein/IL-5/CCL11/CCR3/α-SMA/collagen 1 in the hearts of both T. spiralis-infected mice and T. spiralis-infected mice with blockage of galectin-receptor interactions. Our data suggest that galectin-receptor interactions play a pivotal role during acute T. spiralis infection, and lack of galectin-receptor interactions upregulates Gal-3 which, in turn, leads to elevated heart eosinophil recruitment, exacerbated heart pathology and fibrosis, and heart functional damage.

The Apoptotic Effect of Trichinella spiralis Infection Against Experimentally Induced Hepatocellular Carcinoma.

BACKGROUND: Hepatocellular carcinoma (HCC) is the sixth most common type of cancer. Prognosis of HCC remains unsatisfactory. Therefore, developing new therapeutic modalities is still mandatory. Tumor biotherapy is a novel concept developed as a therapeutic strategy for cancer treatment. There is a similarity between the regulatory mechanism of Trichinella spiralis nurse cell formation and tumor cell apoptosis signal regulation. OBJECTIVES: Induction of apoptosis by T. spiralis can represent a new strategy for tumor treatment. METHODS: Experimental animals were divided in four groups; negative control (GI), T. spiralis infected (GII), induced HCC (GIII) and HCC then infected with T. spiralis (GIV). The apoptotic effect of T. spiralis infection was assessed by histopathological and immunohistochemical staining of B-cell lymphoma 2 (Bcl-2). RESULTS: We found higher survival rate of rats and decreased weight of their livers with no nodules in HCC- T. spiralis group as compared to HCC group. Improvement of the dysplastic changes and increased apoptotic bodies which was confirmed by decreased expression of Bcl-2 reported in HCC- T. spiralis group. CONCLUSION: Trichinella-induced apoptosis can be a contributing mechanism of the anti-tumor effect of T. spiralis infection. Our results showed a certain level of decreased progression of the tumor in HCC-T. spiralis group as indicated by increased rate of apoptosis and subsequently had a positive impact on the survival of rats.
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Induction of the IL-10-producing regulatory B cell phenotype following Trichinella spiralis infection.

Regulatory B cells (Bregs), a subset of B lymphocytes discovered in the past few decades, have the capacity to suppress the immune response and dampen inflammation by secreting cytokines (IL-10 and TGF-ß). Whether Bregs are involved in Trichinella spiralis infection and the phenotypic characteristics of these cells after infection are still unknown. We investigated the phenotype of and dynamic changes in IL-10-producing Bregs in Trichinella spiralis infection in BALB/c mice. We used multicolour fluorescence immunostaining of microwave-treated paraffin sections to investigate the number of Bregs in T. spiralis infection. Flow cytometry (FCM) was used to determine the frequency of Bregs and related subgroups and cytokines in the spleen and mesenteric lymph nodes (MLNs). High levels of IL-10 were detected in the spleen and MLNs of mice after infection with T. spiralis. Furthermore, the frequencies of IL-10-producing CD19+CD1dhighCD5+ regulatory B cells and CD19+ cells were increased during T. spiralis infection. We also showed that the induced phenotype was similar to that of transitional type 2 marginal zone precursor B cells (T-MZP) cells after T. spiralis infection in mice. This study is the first demonstration of the expansion of Bregs following T. spiralis infection.

Comparative multi-omics analyses reveal differential expression of key genes relevant for parasitism between non-encapsulated and encapsulated Trichinella.

Genome assemblies provide a powerful basis of comparative multi-omics analyses that offer insight into parasite pathogenicity, host-parasite interactions, and invasion biology. As a unique intracellular nematode, Trichinella consists of two clades, encapsulated and non-encapsulated. Genomic correlation of the distinct differences between the two clades is still unclear. Here, we report an annotated draft reference genome of non-encapsulated Trichinella, T. pseudospiralis, and perform comparative multi-omics analyses with encapsulated T. spiralis. Genome and methylome analyses indicate that, during Trichinella evolution, the two clades of Trichinella exhibit differential expansion and methylation of parasitism-related multi-copy gene families, especially for the DNase II members of the phospholipase D superfamily and Glutathione S-transferases. Further, methylome and transcriptome analyses revealed divergent key excretory/secretory (E/S) genes between the two clades. Among these key E/S genes, TP12446 is significantly more expressed across three life stages in T. pseudospiralis. Overexpression of TP12446 in the mouse C2C12 skeletal muscle cell line could induce inhibition of myotube formation and differentiation, further indicating its key role in parasitism of T. pseudospiralis. This multi-omics study provides a foundation for further elucidation of the mechanism of nurse cell formation and immunoevasion, as well as the identification of pharmacological and diagnostic targets of trichinellosis.

Oxidative stress mediated apoptotic potential of mefloquine on experimental trichinellosis.

Conventional anthelmintics such as albendazole could not achieve complete cure of trichinellosis till now. The antimalarial mefloquine mediates oxidative stress and disrupts lysosomal functions leading to cell death. Therefore, the aim of this work was to investigate the effect of mefloquine on experimental acute and chronic trichinellosis and to clarify the possible mechanisms of such effects. Mice were divided into four groups; Group I: Uninfected untreated control (20 mice); Group II: Infected untreated control (40 mice); Group III: infected and treated with albendazole (400 mg/kg) (40 mice); Group IV: infected and treated with mefloquine (300 mg/kg) (40 mice). All infected treated groups were equally subdivided into 2 subgroups; (a) treated on the 2nd day post infection (dpi) for 3 days, (b) treated on the 35th dpi for 5 days. Parasitological adults and larvae counting besides immunohistopathological examination of intestines and muscles were done. Biochemical assay of oxidant/antioxidant status, apoptotic, cytoprotective and inflammatory biomarkers in intestinal and muscle homogenates were achieved. Results showed that both albendazole and mefloquine significantly reduced adults and larvae counts with higher efficacy of albendazole in the intestinal phase and superiority of mefloquine in the muscle phase. The superiority of mefloquine was indicated by increased inflammatory immune infiltration and decreased anti-apoptotic immunohistochemical markers expression in both jejunal and muscle tissues. Biochemically, mefloquine treatment showed highly significant oxidative, apoptotic and inflammatory effects. So, our results suggest that mefloquine might be a superior treatment for chronic trichinellosis.

Trichinella spiralis co-infection exacerbates Plasmodium berghei malaria-induced hepatopathy.

BACKGROUND: Although Plasmodium parasites and intestinal helminths share common endemic areas, the mechanisms of these co-infections on the host immune response remain not fully understood. Liver involvement in severe Plasmodium falciparum infections is a significant cause of morbidity and mortality. However, the effect of pre-existing Trichinella spiralis infection on the immune response and liver immune-pathogenesis in P. berghei ANKA (PbANKA)-infected mice needs to be elucidated. METHODS: Outbred Kunming mice were infected with T. spiralis and 9 days later were challenged with P. berghei ANKA (PbANKA), and the investigation occurred at 13 days after co-infection. RESULTS: Compared with PbANKA-mono-infected mice, T. spiralis + PbANKA-co-infected mice had similar survival rate but lower PbANKA parasitaemia; however, there were more severe hepatosplenomegaly, increased liver and spleen indexes, and increased liver pathology observed by hematoxylin and eosin staining; higher expression levels of galectin (Gal)-1, Gal-3, CD68+ macrophages, and elastase-positive neutrophils measured by immunohistochemical staining; upregulated mRNA expression levels of Gal-1, Gal-3, cytokines (interferon-gamma (IFNγ) and interleukin (IL)-6), and M1 macrophage polarization marker (inducible nitric oxide synthase (iNOS)) in the liver, and increased expression levels of Gal-1, IFNγ, IL-6, eosinophil cationic protein, eosinophil protein X, and M1 (IL-1ß and iNOS) and M2 (Ym1) macrophage polarization markers in the spleen of co-infected mice detected by using quantitative real-time reverse transcription polymerase chain reaction (qRT-PCR). In vitro study showed that compared with PbANKA-mono-infected mice, there were significantly increased expression levels of Gal-1, Gal-3, IL-6, IL-1ß, and iNOS in the peritoneal macrophage isolated from co-infected mice detected by using qRT-PCR. Correlation analysis revealed significant positive correlations between Gal-3 and IL-1ß in the peritoneal macrophages isolated from PbANKA-mono-infected mice, between Gal-3 and IFNγ in the spleen of co-infected mice, and between Gal-1 and Ym1 in the peritoneal macrophages isolated from co-infected mice. CONCLUSIONS: Our data indicate that pre-existing infection of T. spiralis may suppress P. berghei parasitaemia and aggravate malaria-induced liver pathology through stimulating Gal-1 and Gal-3 expression, activating macrophages, neutrophils, and eosinophils, and promoting mediator release and cytokine production.

Trichinella spiralis-induced mastocytosis and erythropoiesis are simultaneously supported by a bipotent mast cell/erythrocyte precursor cell.

Anti-helminth responses require robust type 2 cytokine production that simultaneously promotes worm expulsion and initiates the resolution of helminth-induced wounds and hemorrhaging. However, how infection-induced changes in hematopoiesis contribute to these seemingly distinct processes remains unknown. Recent studies have suggested the existence of a hematopoietic progenitor with dual mast cell-erythrocyte potential. Nonetheless, whether and how these progenitors contribute to host protection during an active infection remains to be defined. Here, we employed single cell RNA-sequencing and identified that the metabolic enzyme, carbonic anhydrase (Car) 1 marks a predefined bone marrow-resident hematopoietic progenitor cell (HPC) population. Next, we generated a Car1-reporter mouse model and found that Car1-GFP positive progenitors represent bipotent mast cell/erythrocyte precursors. Finally, we show that Car1-expressing HPCs simultaneously support mast cell and erythrocyte responses during Trichinella spiralis infection. Collectively, these data suggest that mast cell/erythrocyte precursors are mobilized to promote type 2 cytokine responses and alleviate helminth-induced blood loss, developmentally linking these processes. Collectively, these studies reveal unappreciated hematopoietic events initiated by the host to combat helminth parasites and provide insight into the evolutionary pressure that may have shaped the developmental relationship between mast cells and erythrocytes.

Primary characterization of the immune response in pigs infected with Trichinella spiralis.

Trichinellosis, which is caused by Trichinella spiralis (T. spiralis), is a serious zoonosis. Pigs play an important role in the transmission of human trichinellosis. Characterizing the immune response to T. spiralis infection is key to elucidating host-parasite interactions. However, most studies on the immune response to T. spiralis infection have employed murine models. In this study, we investigated the immune response to T. spiralis infection in pigs. The results showed that the average numbers of larvae per gram (lpg) for the 100-muscle larvae (ML), 1000-ML, and 10 000-ML groups were 1.502, 35.947, and 398.811, respectively. The percentages of CD3+ T cells, B cells, CD4+ T cells, Treg cells, and Th17 cells were elevated in the infection groups compared to the control animals. In contrast, CD8+ T cell percentages were reduced after infection in the low-dose group. The number of neutrophils was increased at 3-17 days post-infection (dpi). Th1 cytokine IL-2 levels were significantly decreased at 7 dpi, and Th2 cytokine IL-4 levels were significantly elevated at 3 dpi. Treg cytokine IL-10 levels were significantly elevated between 7 dpi and 30 dpi. Th17 cytokine IL-17A levels were significantly increased beginning at 11 dpi. These results confirmed that pigs infected with T. spiralis predominantly induced Th2 and Treg immune responses, which suppress the Th1 immune responses. This study provides novel insights into the immune response of pigs infected with T. spiralis.

Vaccination of mice with a recombinant novel cathepsin B inhibits Trichinella spiralis development, reduces the fecundity and worm burden.

BACKGROUND: Trichinella spiralis is a major zoonotic tissue-dwelling nematode, which is a public health concern and a serious hazard to animal food safety. It is necessary to exploit an anti-Trichinella vaccine to interrupt the transmission of Trichinella infection among animals and from animals to humans. The purpose of the present study was to characterize the novel T. spiralis cathepsin B (TsCB) and to evaluate the immune protection elicited by immunization with recombinant TsCB (rTsCB). METHODS: The complete cDNA sequences of the TsCB gene were cloned, expressed and purified. The antigenicity of rTsCB was investigated by western blot analysis and ELISA. Transcription and expression of TsCB at various T. spiralis life-cycle stages were analyzed by RT-PCR and indirect immunofluorescent assay (IIFA). The mice were subcutaneously immunized with rTsCB, and serum level of TsCB-specific IgG (IgG1 and IgG2a) and IgE antibodies were assayed by ELISA. Immune protection elicited by vaccination with rTsCB was investigated. RESULTS: The TsCB was transcribed and expressed in four T. spiralis life-cycle stages (adult worm, AW; newborn larvae, NBL; muscle larvae, ML; and intestinal infective L1 larvae), it was primarily located in the cuticle and stichosome of the parasitic nematode. Vaccination of mice with rTsCB produced a prominent antibody response (high level of specific IgG and IgE) and immune protection, as demonstrated by a 52.81% AW burden reduction of intestines at six days post-infection (dpi) and a 50.90% ML burden reduction of muscles at 35 dpi after oral larva challenge. The TsCB-specific antibody response elicited by immunization with rTsCB also impeded intestinal worm growth and decreased the female fecundity. CONCLUSIONS: TsCB might be considered as a novel potential molecular target to develop vaccines against T. spiralis infection.

Possible case of trichinellosis associated with beaver (Castor fiber) meat.

Although there have been occasional reports of rare and low-level trichinellae infestation in beavers, no human cases of beaver-associated trichinellosis have been described. This report presents a possible case of human trichinellosis linked to beaver meat. Increasing consumption of beaver meat necessitates raising awareness of this potential source of trichinellosis.

Border zone brain lesions due to neurotrichinosis.

Trichinosis is a parasitic disease that, due to variable clinical syndromes, is often underrecognized. We present the case of a patient with eosinophilia, focal neurological signs and multiple bilateral brain lesions, distributed mainly in the border zones. The diagnostic workup revealed neurotrichinosis, which should be suspected even without a clear history of consumption of poorly cooked meat.

Oral contraceptive pills: Risky or protective in case of Trichinella spiralis infection?

The aim of this study was to investigate how Trichinella spiralis infection can be affected by contraceptive pills in vivo. Methods included six groups of female Wistar rats; healthy, Trichinella infected, receiving combined contraceptive pills (COCPs), receiving progestin only pills (POPs), infected receiving COCPs and infected receiving POPs. Parasite burden was measured; adult worm counts, gravidity, larvae and reproductive capacity index). Histopathological examination, immunohistochemical detection of C-kit+ mast cells and Foxp3+ T-reg. cells in intestinal sections, eosinophils muscle infiltration and CPK level were performed. Rats infected and receiving COCPs showed a significant increase in parasitic burden, and infected receiving POPs showed a significant reduction compared to infected only, with a significant increase in nongravid females (Mean total worms=964.40±55.9, 742±52.63, 686±31.68, larvae/g=5030±198.75, 2490±143.18 and 4126±152,91, respectively). Intestinal sections from infected receiving COCPs showed intact mucosa (though the high inflammatory cells infiltrate), and significant increase in C-kit+ mast cells number and intensity (30.20±4.15 and 60.40±8.29), and Foxp3+ T-reg. cells (10±1.58). Infected receiving POPs showed a significantly less CPK (5886±574.40) and eosinophilic muscle infiltration (58±13.51). Oestrogen-containing pills established a favourable intestinal environment for Trichinella by enhancing Foxp+T-reg. cells and stabilizing C-kit+mast cells, while POPs gave a potential protection with less gravidity, larval burden and eosinophilic infiltrate.

Transfer of CD11c+ lamina propria mononuclear phagocytes from post-infectious irritable bowel syndrome causes mucosal barrier dysfunction and visceral hypersensitivity in recipient mice.

The role of low-grade inflammation in the development of post­infectious irritable bowel syndrome (PI­IBS) has attracted increasing attention. Abnormal CD11c+ mononuclear phagocytes, such as dendritic cells (DCs), macrophages, and monocytes, are involved in the disruption of immune tolerance in organisms, which can lead to the development of chronic inflammatory diseases. The present study tested the hypothesis that CD11c+ lamina propria mononuclear phagocytes (CD11c+ LPMPs) contribute to increased mucosal permeability and visceral hypersensitivity in a PI­IBS mouse model. CD11c+ LPMPs were isolated and purified via the digestion of intestinal tissues and magnetic­activated cell sorting. We detected increased mucosal permeability, visceral hypersensitivity and intestinal inflammation during both the acute and chronic stages of Trichinella infection. Following the transfer of CD11c+ LPMPs from PI­IBS mice into normal mice, low­grade inflammation was detected, as demonstrated by increased IL­4 expression in the ileum, as well as enhanced mucosal permeability, as indicated by decreased transepithelial electrical resistance and the pre-sence of ultrastructural alterations. More importantly, the mice that underwent adoptive transfer of CD11c+ LPMPs from the PI­IBS mice also exhibited increased abdominal withdrawal reflex scores and a decreased threshold. Our data demonstrated that the CD11c+ LPMPs from this PI­IBS mouse model were not only able to transfer enteric inflammation to the normal mice but also caused abnormal intestinal function, characterized by epithelial barrier disruption and visceral hyperalgesia.

Innate immunity modulation in the duodenal mucosa induced by REM sleep deprivation during infection with Trichinella spirallis.

Sleep is considered to be an important predictor of the immunity, since the absence of sleep can affect the development of the immune response, and consequently increase the susceptibility to contract an infection. The aim of the present study was to investigate if sleep deprivation and stress induce dysregulation of the duodenal mucous membrane during the acute infection with Trichinella spiralis. Our results shows that, in the intestinal mucous membrane, stress and sleep deprivation, produces different effect in the cells, and this effect depends on the studied duodenal compartment, glands or villi. The sleep deprivation affect mast cells mainly, and the stress response is more heterogeneous. Interestingly, in the duodenal mucous membrane, none population of cells in the infected groups responded equally to both conditions. These findings suggest that the response of the intestinal mucous membrane during the infection caused for T. spiralis turns out to be affected in the sleep-deprived rats, therefore, the results of the present study sustain the theory that sleep is a fundamental process that is capable of modulating the immune response of mucous membranes, particularly the one generated against the parasite Trichinella spiralis.

Implication of artemisinin nematocidal activity on experimental trichinellosis: In vitro and in vivo studies.

Benzimidazole drugs are used for treatment of trichinellosis, but they have a limited effect against encapsulated larval stages of Trichinella spiralis. Hence, there is a considerable interest in developing new anthelmintic drugs. Our aim is to investigate the possible effect of artemisinin on T. spiralis in in vitro and in vivo studies. T. spiralis worms were isolated from infected mice and transferred to 3 culture media; group I: with no drugs, group II: contained artemisinin and group III: contained mebendazole, then they were subjected to electron microscopic study. An in vivo study was done where mice were divided into three groups; group I: infected and untreated, group II: received artemisinin and group III: received mebendazole. The efficacy of treatment was assessed by adult and total larval counts, histopathological study of the small intestinal and muscle tissues and immunohistochemical staining of cyclooxygenase-2 (COX-2) and vascular endothelial growth factor (VEGF) in muscles. Adult worm teguments showed significant degeneration and destruction with both drugs. Also, significant reduction of total adult and larval counts occurred in treated groups in comparison to the control group. Histopathological examination of the small intestine and muscles showed marked improvement with reduction in the inflammatory infiltrates with both drugs. COX-2 and VEGF expressions were reduced in both treated groups with more reduction in the artemisinin-treated group. This study revealed that artemisinin has the potential to be an alternative drug against trichinellosis.

A Large-Scale Survey of Trichinella spp. Infection in Japanese Wild Boars.

This study presents the results of a large-scale, one-year survey of Trichinella spp. in Japanese wild boars (Sus scrofa). We analyzed the tongues of 1,168 wild boars captured by hunters in 30 prefectures of Japan, most of which were boar habitats, from October 2014 to January 2015. The samples were digested, and the prevalence of Trichinella spp. muscle larvae was examined. Examination of pooled samples from 10 individuals (15 g per head) or 117 randomly selected samples (10% of the total number of samples) that were individually processed showed no larval infection. Thus, our data suggests that Japanese wild boars do not play a major role in the sylvatic cycle of Trichinella parasites.