First case of human neurocoenurosis caused by Taenia serialis: A case report.

Human coenurosis is caused by the larval stages of Taenia species, mainly Taenia multiceps and Taenia serialis. T. multiceps has been reported to cause human central nervous system (CNS) infections, but no CNS case caused by T. serialis has been reported. The authors report the first case of human neurocoenurosis caused by T. serialis, which was confirmed by mitochondrial DNA analysis. A 38-year-old man presented with visual disturbance and headache, and subsequent magnetic resonance imaging (MRI) revealed a ring-enhancing cystic lesion in the left occipital lobe. Biopsy was performed, and the resultant histopathological diagnosis was that of low-grade B-cell lymphoma. Chemotherapy was initiated, but a subsequent MRI showed increased ring enhancement. Due to the unexpected clinical course, a surgical resection of the lesion was performed. The lesion was completely removed. Pathological examination showed multiple scolices with hooklets, suckers, and numerous calcareous corpuscles. Therefore, the diagnosis of neurocysticercosis was made. However, mitochondrial DNA analysis showed that the disease was definitively coenurosis caused by T. serialis. Albendazole was administered, with no evidence of recurrence at 12 months following the operation. In this study, we demonstrate that T. serialis can cause CNS infection and that genetic analysis is recommended to establish a definitive diagnosis.

Hippocampal sclerosis induced in mice by a Taenia crassiceps metacestode factor.

An experimental Taenia crassiceps mouse model was used to assess the role of Taenia solium metacestode factor (Fac) in human neurocysticercosis. Intraperitoneal infection with T. crassiceps metacestodes or subcutaneous inoculation with a T. crassiceps metacestode factor (Fac) produced significant impairment of performance (learning) in the Barnes maze and induced bilateral hippocampal sclerosis in mice. Several staining techniques revealed important cell dispersion, extensive apoptosis and cell loss in the dentate gyrus, hilus and CA1-CA3 regions of both hippocampi, as well as intense deterioration of the adjacent cortex. An outstanding disruption of its histoarchitecture in the surrounding tissue of all these regions and apoptosis of the endothelial cells were also observed.

Co-infection: the outcome of Plasmodium infection differs according to the time of pre-existing helminth infection.

Although helminth-Plasmodium coinfections are common in tropical regions, the implications of this co-existence for the host immune response are poorly understood. In order to understand the effect of helminth infection at different times of coinfection on the immune response against Plasmodium infection, BALB/c mice were intraperitoneally infected with Taenia crassiceps (Tc). At 2 (Tc2) or 8 (Tc8) weeks post-infection, mice were intravenously infected with 1 × 103 Plasmodium yoelii (Py) 17XL-parasitized red blood cells. Py 17XL-single-infected mice developed cachexia, splenomegaly, and anemia, and died at 11 days post-infection. Importantly, Tc2 + Py-coinfected mice showed increased survival of 58% on day 11, but developed pathology (cachexia and splenomegaly) and succumbed on day 18 post-coinfection, this latter associated with high levels of IL-1ß and IL-12, and reduced IFN-γ in serum compared with Py 17XL-single-infected mice. Interestingly, Tc8 + Py-coinfected mice showed increased survival up to 80% on day 11 and succumbed on day 30 post-coinfection. This increased survival rate conferred by chronic helminth infection was associated with a decreased pathology and mixed inflammatory-type 1/anti-inflammatory-type 2 immune profile as evidenced by the production of high levels of IL-12 and IL-10, and reduced TNF-α from macrophages, high levels of IL-4 and IL-10, and low levels of IFN-γ from spleen cells. Also high serum levels of IL-1ß, TNF-α, IL-12, IL-4, and IL-10, but a significant reduction of IFN-γ were observed. Together, these data indicate that polarization of the cell-mediated response modulated by a pre-existing helminth infection differentially impacts on the host immune response to Py 17XL in a time-dependent manner.

Granulomatous responses in larval taeniid infections.

Granulomas are responses to persistent nonliving bodies or pathogens, centrally featuring specialized macrophage forms called epithelioid and multinucleated giant cells. The larval stages of the cestode parasites of the Taeniidae family (Taenia, Echinococcus) develop for years in fixed tissue sites in mammals. In consequence, they are targets of granulomatous responses. The information on tissue responses to larval taeniids is fragmented among host and parasite species and scattered over many decades. We attempt to draw an integrated picture of these responses in solid tissues. The intensity of inflammation around live parasites spans a spectrum from minimal to high, parasite vitality correlating with low inflammation. The low end of the inflammatory spectrum features collagen capsules proximal to the parasites and moderate distal infiltration. The middle of the spectrum is dominated by classical granulomatous responses, whereas the high end features massive eosinophil invasions. Across the range of parasite species, much observational evidence suggests that eosinophils are highly effective at killing larval taeniids in solid tissues, before and during chronic granulomatous responses. The evidence available also suggests that these parasites are adapted to inhibit host granulomatous responses, in part through the exacerbation of host regulatory mechanisms including regulatory T cells and TGF-ß.

Prevalence of Echinococcus granulosus taeniasis in stray dogs in the region of Constantine (North-East Algeria).

In North Africa, the domestic dog is regarded as the main reservoir for infection by Echinococcus granulosus of domestic livestock and man. In Algeria, there is very little data on the rate of infestation of dogs, while the prevalence of E. granulosus in the definitive host is a very reliable marker of the potential risk of transmission of cystic tapeworm to humans and livestock. To find out this information, a survey was conducted to assess the prevalence of infection with E. granulosus in stray dogs in the region of Constantine (North-East Algeria). We autopsied and examined 120 stray dogs, 22 (18.3%) of which were infected with E. granulosus, with an average intensity of infestation of 249 worms. The prevalence in the area of survey was evaluated: 15.5% (14/90) and 26.6% (8/30) dogs were parasitized by E. granulosus in urban and rural areas respectively. The influence of age on the rate of infection was very marked. In addition, the appreciation of the prevalence of parasitism by cestodes as a whole showed that 56 (46.6%) animals out of 120 were infected. Facing such a situation of endemic tapeworm parasitism, with a potential risk of transmission to humans, there is an urgent need to take measures to control and break the epidemiological cycles of the parasite.

Gross, histopathological and immunohistochemical study on strobilocercus of Taenia taeniaeformis infection in the liver of laboratory rats (Rattus norvegicus) in India.

We report the detailed gross, histopathological and immunohistochemical study of Strobilocercus fasciolaris infection, the metacestodal stage of Taenia taeniaeformis, in the liver of laboratory Wistar rats. Necropsy examination of seventeen rats revealed transparent or white or cream to clear, thick walled cysts, 1 to 97 in number, measuring about 2mm to 12mm on one or many of the liver lobes and containing strobilocercus of Taenia taeniaeformis. Histopathological examination revealed the presence of the cross-section of larva surrounded by a thick fibrous capsule and moderate infiltration of lymphocytes, plasma cells and a few eosinophils. Fatty degeneration of hepatocytes, gastric mucosal hyperplasia, distended gastric glands and marked increase in the mucosal epithelial cells and goblet cells in the duodenum were also observed. Contamination of feed and bedding materials seems to be the probable source in these naturally infected rats.

A non-hepatotropic parasite infection increases mortality in the acetaminophen-induced acute liver failure murine model: possible roles for IL-5 and IL-6

We evaluated the effects of a non-hepatotropic parasite infection (Taenia crassiceps) on the outcome of acetaminophen-induced acute liver failure in mice. Uninfected and T. crassiceps infected mice orally received either 300 mg/kg acetaminophen or water as vehicle (n = 5 per group). Survival analysis, hepatocyte necrosis, alanine aminotransferase (ALT) levels, CYP2E1 protein, interleukin (IL-) 5, and IL-6 were assessed for all groups. All infected mice died within 16 h after exposure to acetaminophen (Tc+APAP group), whereas only one-third of uninfected animals exposed to acetaminophen (APAP group) died. Uninfected (Control group) and infected (Tc group) mice that received the vehicle showed no liver damage. Tc+APAP mice exhibited massive liver necrosis characterised by marked balloning degeneration of hepatocytes and higher serum ALT compared to Control, Tc, and APAP animals. Liver tissue from Tc+APAP mice also displayed increased expression of CYP2E1 protein and higher mRNA and protein levels of IL-5 and IL-6 compared to the other groups. These findings suggest that non-hepatotropic parasite infections may increase mortality following acute liver failure by promoting hepatocyte necrosis via IL-5 and IL-6-dependent CYP2E1 overproduction. This study identifies new potential risk factors associated with severe acute liver failure in patients.

A non-hepatotropic parasite infection increases mortality in the acetaminophen-induced acute liver failure murine model: possible roles for IL-5 and IL-6.

We evaluated the effects of a non-hepatotropic parasite infection (Taenia crassiceps) on the outcome of acetaminophen-induced acute liver failure in mice. Uninfected and T. crassiceps infected mice orally received either 300 mg/kg acetaminophen or water as vehicle (n = 5 per group). Survival analysis, hepatocyte necrosis, alanine aminotransferase (ALT) levels, CYP2E1 protein, interleukin (IL-) 5, and IL-6 were assessed for all groups. All infected mice died within 16 h after exposure to acetaminophen (Tc+APAP group), whereas only one-third of uninfected animals exposed to acetaminophen (APAP group) died. Uninfected (Control group) and infected (Tc group) mice that received the vehicle showed no liver damage. Tc+APAP mice exhibited massive liver necrosis characterised by marked balloning degeneration of hepatocytes and higher serum ALT compared to Control, Tc, and APAP animals. Liver tissue from Tc+APAP mice also displayed increased expression of CYP2E1 protein and higher mRNA and protein levels of IL-5 and IL-6 compared to the other groups. These findings suggest that non-hepatotropic parasite infections may increase mortality following acute liver failure by promoting hepatocyte necrosis via IL-5 and IL-6-dependent CYP2E1 overproduction. This study identifies new potential risk factors associated with severe acute liver failure in patients.

Pathogenesis of Taenia solium taeniasis and cysticercosis.

Taenia solium infections (taeniasis/cysticercosis) are a major scourge to most developing countries. Neurocysticercosis, the infection of the human nervous system by the cystic larvae of this parasite, has a protean array of clinical manifestations varying from entirely asymptomatic infections to aggressive, lethal courses. The diversity of clinical manifestations reflects a series of contributing factors which include the number, size and location of the invading parasites, and particularly the inflammatory response of the host. This manuscript reviews the different presentations of T. solium infections in the human host with a focus on the mechanisms or processes responsible for their clinical expression.

Co-infection with Enterobius vermicularis and Taenia saginata mimicking acute appendicitis.

In this report, we describe an unusual case of verminous appendicitis due to Enterobius vermicularis and Taenia saginata in a 29-year-old woman from Iran. The histopathological examinations and parasitological descriptions of both worms found in the appendix lumen are discussed. The removed appendix exhibited the macroscopic and microscopic features of acute appendicitis. Antihelminthic therapy was initiated with single doses of praziquantel for the taeniasis and mebendazole for the enterobiasis, and the patient was discharged.

A Taenia crassiceps factor induces apoptosis of spleen CD4+T cells and TFG-ß and Foxp3 gene expression in mice.

This study was undertaken to determine whether a parasite substance produces structural pathology in the mouse spleen. A low-molecular-weight Taenia crassiceps metacestode factor (MF) isolated from the peritoneal fluid of female mice infected with T. crassiceps metacestodes induced pathological and immunological changes in mouse spleen cells in vivo. Electron microscopy and confocal microscopy revealed severe changes in the spleen histoarchitecture of T. crassiceps-infected and MF-treated mice. Apoptotic degenerated spleen cells were observed in the white and red pulps and were more conspicuous in the white pulp of the spleen from the T. crassiceps-infected mice than in that of the MF-treated mice. Flow cytometry analysis revealed that the numbers of spleen CD4+T cells were significantly lower in both experimental groups than in control mice. The ex vivo expression of transforming growth factor (TGF)-ß and factor Foxp3 were significantly higher in splenocytes of the experimental mice than the basal expression observed in the control cells. These findings may have potential applications for a better understanding of the host-parasite relationship in human neurocysticercosis.

Cytokine, antibody and proliferative cellular responses elicited by Taenia solium calreticulin upon experimental infection in hamsters.

Taenia solium causes two diseases in humans, cysticercosis and taeniosis. Tapeworm carriers are the main risk factor for neurocysticercosis. Limited information is available about the immune response elicited by the adult parasite, particularly the induction of Th2 responses, frequently associated to helminth infections. Calreticulin is a ubiquitous, multifunctional protein involved in cellular calcium homeostasis, which has been suggested to play a role in the regulation of immune responses. In this work, we assessed the effect of recombinant T. solium calreticulin (rTsCRT) on the cytokine, humoral and cellular responses upon experimental infection in Syrian Golden hamsters (Mesocricetus auratus). Animals were infected with T. solium cysticerci and euthanized at different times after infection. Specific serum antibodies, proliferative responses in mesenteric lymph nodes and spleen cells, as well as cytokines messenger RNA (mRNA) were analyzed. The results showed that one third of the infected animals elicited anti-rTsCRT IgG antibodies. Interestingly, mesenteric lymph node (MLN) cells from either infected or non-infected animals did not proliferate upon in vitro stimulation with rTsCRT. Additionally, stimulation with a tapeworm crude extract resulted in increased expression of IL-4 and IL-5 mRNA. Upon stimulation, rTsCRT increased the expression levels of IL-10 in spleen and MLN cells from uninfected and infected hamsters. The results showed that rTsCRT favors a Th2-biased immune response characterized by the induction of IL-10 in mucosal and systemic lymphoid organs. Here we provide the first data on the cytokine, antibody and cellular responses to rTsCRT upon in vitro stimulation during taeniasis.

A Taenia crassiceps metacestode factor enhances ovarian follicle atresia and oocyte degeneration in female mice.

The histopathological effects of Taenia crassiceps infection or T. crassiceps metacestode factor inoculation on the mouse ovary were determined using six female mice in three groups: infected mice, mice inoculated with the metacestode factor and control mice. The control group was subcutaneously inoculated with healthy peritoneal fluid. The infected group was intraperitoneally inoculated with 40 T. crassiceps metacestodes, and the metacestode factor group was subcutaneously inoculated with T. crassiceps metacestode factor (MF). Light and electron microscopy and TUNEL (terminal deoxynucleotidyl transferase (TdT)-mediated dUTP nick end labelling) assays revealed a significant increase in ovarian follicular atresia (predominantly in antral/preovulatory stages of development), oocyte degeneration (P< 0.05), and a decrease in the amount of corpus luteum in follicles of mice infected and inoculated with MF compared with the control group. Significant abnormalities of the granulosa cells and oocytes of the primordial, primary and secondary ovarian follicles occurred in both treated mouse groups (P< 0.05) compared with no degeneration in the control group. These pathological changes in female mice either infected with T. crassiceps metacestodes or inoculated with T. crassiceps MF may have consequences for ovulation and fertility.

Distribution and histopathological changes induced by cysts of Taenia solium in the brain of pigs from Tanzania.

Neurocysticercosis (NCC) caused by Taenia solium cysts is a frequent but neglected parasitic disease of the central nervous system (CNS) worldwide. The aim of this study was to describe anatomical locations of cysts in the CNS and the corresponding inflammation. A total of 17 naturally infected pigs were used to evaluate the distribution of cysts and, of these, seven were used to evaluate the corresponding inflammation further, through histopathology. Clinical signs in the pigs included dullness, sluggishness, somnolence, apathy and loss of consciousness. Cysts were distributed in all cerebral lobes, i.e. 39.7% in the frontal lobe, 20.3% in the parietal lobe, 20.0% in the occipital lobe and 19.7% in the temporal lobe, and only 0.4% in the cerebellum. No cysts were found in the spinal cord. Cysts were localized as follows: 47.9% in the dorsal subarachnoid, 46.9% in the parenchyma, 4.4% in the subarachnoid base and 0.9% in the ventricles. The results of the histopathology revealed lesions in an early inflammatory stage, i.e. stage I, in all anatomical locations except for two, which showed more of an inflammatory reaction, stage III, in one pig. It was concluded that clinical signs in pigs were neither pathognomonic nor consistent. These signs, therefore, cannot be used as a reliable indicator of porcine NCC. Furthermore, T. solium cysts were found to be in abundance in all cerebral lobes, and only a few were found in the cerebellum. Regarding the inflammatory response, no significant differences were found in the location and total number of cysts. Thus, further studies are needed to explain the determinants of cyst distribution in the CNS and assess in detail clinical signs associated with porcine NCC.

Immunology of Taenia solium taeniasis and human cysticercosis.

The life cycle of Taenia solium, the pork tapeworm, is continuously closed in many rural settings in developing countries when free roaming pigs ingest human stools containing T. solium eggs and develop cysticercosis, and humans ingest pork infected with cystic larvae and develop intestinal taeniasis, or may also accidentally acquire cysticercosis by faecal-oral contamination. Cysticercosis of the human nervous system, neurocysticercosis, is a major cause of seizures and other neurological morbidity in most of the world. The dynamics of exposure, infection and disease as well as the location of parasites result in a complex interaction which involves immune evasion mechanisms and involutive or progressive disease along time. Moreover, existing data are limited by the relative lack of animal models. This manuscript revises the available information on the immunology of human taeniasis and cysticercosis.

[Acute appendicitis and coinfection with enterobiasis and taeniasis: a case report]. / Akut apandisit ve enterobiyaz ile taeniyaz: bir olgu sunumu.

Parasites are rarely associated with inflammation of the appendix. Generally, parasites cause acute abdominal pain via blocking the gut lumen. In this article, we presented a case of appendicitis where Enterobius vermicularis was detected in the surgical specimen and Taenia was detected in the stool. A 31 year old male patient was admitted to the emergency room with severe abdominal pain, which has begun two days ago. On physical examination, tenderness was positive on palpation of the right lower abdominal quadrant and the patient was operated on with the diagnosis of acute appendicitis. Histopathological examination of the patient's appendectomy material revealed numerous parts of parasites resembling Enterobius vermicularis and slight mucosal erosion. On parasitological examination of the patient's stool, Taenia eggs and adult forms were determined. Antiparasitic therapy was started with niclosamide for taeniasis and albendazole for enterobiasis. Parasitic infections can mimic acute appendicitis clinically. Radiological and laboratory findings do not help to distinguish the diagnosis of acute appendicitis. In the histopathological examination of the appendix, the findings of acute inflammation of the appendix wall may not be defined. For patients with normal histopathological examination, screening for parasites should be done, and anti-parasitic treatment should be started after appendectomy.

Rare case of disseminated cysticercosis and taeniasis in a Japanese traveler after returning from India.

We report disseminated cysticercosis concurrent with taeniasis in a 31-year-old male Japanese, who had visited India three times and stayed for 1 month each time during the previous 1 year. The patient presented increasing numbers of subcutaneous nodules and expelled proglottids, although numerous cysts were also found in the brain in imaging findings, though no neurological symptoms were observed. Histopathological and serological findings strongly indicated cysticercosis. We found taeniid eggs in his stool by microscopic examination and revealed them as the Indian haplotype of Taenia solium by mitochondrial DNA analysis. We concluded that disseminated cysticercosis was caused by the secondary autoinfection with eggs released from the tapeworm carrier himself. After confirming the absence of adult worms in the intestine by copro-polymerase chain reaction, the patient was successfully treated with albendazole at a dose of 15 mg/kg/day for 28 days. Subcutaneous and intracranial lesions had completely disappeared by the end of the treatment period.

Morphological and molecular characterization of bovine coenurosis in Sardinia, Italy.

Coenurosis is a central nervous system disease of wild and domestic ruminants caused by Coenurus cerebralis, a bladder worm stage of Taenia multiceps). Even in Sardinia island, this metacestode seems to be widespread in sheep (Scala et al. Vet Parasitol 143(3-4):294-298, 2007) where coenurosis is an important health problem (Varcasia et al. Parasitol Res 99(5):622-626, 2006) the last and unique report of coenurosis in cattle was in 1990 (Cubeddu et al. 1990). In the present paper, a case of bovine coenurosis in Sardinia was described 22 years after the first report with a morphological a biomolecular characterization. A 2-year-old Limousine bull was euthanized in the Bolotana (NU) municipality (Central Sardinia). The remote anamnesis achieved from the farmer reporting that the bull showed neurological symptoms from 1 year of age previously classified as nutritional problems by the farm's veterinary. The breeder also says that the bull have by self-produced the skull fracture by hitting a gaff in the farm. The skull was opened and the brain removed and carefully examined showing two coenurus cysts containing clear fluid with numerous scoleces both in the right hemisphere. Morphological features of the cysts and mt-DNA sequencing confirm that the parasites were T. multiceps Coenuri.