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Acute cysticercosis favours rapid and more severe lesions caused by Leishmania major and Leishmania mexicana infection, a role for alternatively activated macrophages.

Parasitic helminths have developed complex mechanisms to modulate host immunity. In the present study we found that previous infection of mice with the cestode Taenia crassiceps favours parasitemia and induces larger cutaneous lesions during both Leishmania major and Leishmania mexicana co-infections. Analysis of cytokine responses into draining lymph nodes indicated that co-infection of T. crassiceps-Leishmania did not inhibit IFN-gamma production in response to Leishmania antigens, but significantly increased IL-4 production. Additionally, anti-Leishmania-specific IgG1 antibodies and total IgE increased in co-infected mice, whereas, IgG2a titers remained similar. Macrophages from Taenia-infected mice displayed increased mRNA transcripts of arginase-1, Ym1, and Mannose Receptor, as well as greater production of urea (all markers for an alternate activation state) compared to macrophages from Leishmania-infected mice. In contrast, lower mRNA transcripts for IL-12p35, IL-12p40, IL-23p19, and iNOS were detected in macrophages obtained from cestode-infected mice compared to uninfected and Leishmania-infected mice after LPS stimulation. The presence of cestode also generated impaired macrophage anti-leishmanicidal activity in vitro, as evidenced by the inability of these macrophages to prevent Leishmania growth compared to macrophages from uninfected mice. This was observed despite the fact that both groups of cells were exposed to IFN-gamma. Flow cytometry showed high IFN-gammaR expression on Taenia-induced macrophages. Thus, lack of response to IFN-gamma is not associated with the absence of its receptor. Our data suggest that cestode infection may favour Leishmania installation by inducing alternatively activated macrophages rather than inhibiting Th1-type responses.

Acute Disease↗

Protection from murine cysticercosis by immunization with a parasite cysteine protease.

Central nervous system infection by Taenia solium cysts causes neurocysticercosis, a common neurological infection in the Third World. We have previously isolated cysteine proteases from Taenia crassiceps and T. solium. In this study, we immunized BALB/c mice with the purified T. solium cysteine protease and challenged them with Taenia crassiceps. Immunized mice had a 72% reduction in parasite burden compared to mice that received no immunization. Immunized mice developed antigen specific lymphocyte proliferation. These data support further studies of the T. solium cysteine protease as a vaccine candidate.

Animals↗

Protection of pigs against Taenia solium cysticercosis using recombinant antigen or in combination with DNA vaccine.

In the present study, we investigated the duration of protection afforded to pigs immunized in two different prime-boost regimens: one is homologus priming and boosting with a protein vaccine, and the other is priming with a DNA vaccine and boosting with the protein vaccine. Groups of pigs that received the same vaccination regimen were then challenged with Taenia solium eggs at 6, 12 or 20 weeks post-immunization (wpi), respectively. The results showed that all vaccinated pigs challenged at 6 or 12 wpi showed significant (P < 0.05) reduction in the development of cysts. When challenged at 20 wpi, pigs primed with the DNA vaccine (pcDNA3-cC1) followed by two boosters of the protein vaccine (GST-cC1) showed significant (P < 0.05) protection against the challenge of T. solium eggs, whereas pigs receiving three injections of the protein vaccine showed no significant protection compared to non-vaccinated controls (P > 0.05). Antibody isotype assays showed that DNA prime-protein boost regimen induced a predominantly IgG2 response, compared to an IgG1 biased response for the protein prime-protein boost regimen. In addition, peripheral blood mononuclear cells (PBMC) obtained from the DNA prime-protein boost group proliferated strongly in response to GST-cC1 protein, and this responsiveness persisted until 20 wpi. Taken together, our data suggest that the use of a prime-boost strategy combining DNA and protein vaccines may be better than protein alone for the longevity of protection against the challenge of T. solium eggs.

Animals↗

The US Centers for Disease Control and Prevention (CDC) and research and control of cysticercosis.

It is generally recognized that it is not possible to adequately protect the health of any nation without addressing infectious disease problems that occur elsewhere in the world. In 2002, the US Centers For Disease Control and Prevention (CDC) developed a revised strategy for consolidating, enhancing, and improving the effectiveness of CDC's efforts to prevent and control infectious diseases on a global scale. Taenia solium is one example of an imported infection disease, which impacts on the health of the US population but requires international coordinated efforts to prevent or limit transmission. This report outlines CDC's refocused global infectious disease strategy and how CDC collaborates in international efforts to eliminate taeniasis/cysticercosis.

Animals↗

Human case management and treatment of cysticercosis.

Disease manifestations due to neurocysticercosis vary markedly and depend upon the location, size and number of cysts as well as the viability or degeneration of cysts and presence, type and degree of host response. Accordingly, the clinical management for each patient should be individualized. Treatment modalities include: (1) larvicidal drugs such as albendazole or praziquantel in patients with viable cysts; (2) corticosteroids or other agents to suppress or prevent the host's immune response; (3) anti-seizure medication(s) to treat or prevent recurrent seizures; (4) surgical interventions; and (5) the use of supportive family, social or health agencies in impaired individuals. Although it is known that larvicidal treatment kills viable cysts that commonly resolve or calcify, the clinical benefit of this treatment in the most common presentations is unproven. However, medical treatment of giant subarachnoid cysts, large parenchymal cysts or orbital cysts causing mass effect has led to definite clinical improvement in uncontrolled trials. Whether there is faster radiological improvement and/or clinical benefit in the treatment of cysts showing signs of inflammation by magnetic resonance imaging (enhancement and/or edema) is like-wise controversial. There is no general understanding when or how to use corticosteroids to suppress natural or treatment-induced inflammation around cysts although their use when inflammation contributes or could be expected to cause undue morbidity or mortality is reasonable. Anti-seizure medication should usually be employed in patients with seizures or patients who may likely develop seizures. Surgical intervention is required to alleviate mass effect, remove some cysts causing obstruction of the ventricles, shunt placement for hydrocephalus, and sometimes for removal and/or decompression of large or critically located cysts before larvicidal treatment.

Adrenal Cortex Hormones↗

Epileptogenic activity of granulomas associated with murine cysticercosis.

Neurocysticercosis, caused by Taenia solium, is a common cause of neurologic disease in developing countries and among immigrants to the United States. Seizures are the most common clinical manifestation of neurocysticercosis. Imaging studies of patients with seizures from neurocysticercosis typically reveal evidence of an inflammatory reaction associated with the parasite or calcified granulomas. This study investigated whether a substance produced by the host granulomatous reaction to the dying parasite, in a mouse model of the infection, is sufficient to induce epileptiform activity. Granulomas associated with Taenia crassiceps cysticerci were removed from the peritoneal cavity of infected mice. One piece of the granuloma was used for blinded histological staging of the dying parasite. The second piece was used to generate extracts, which were injected into the hippocampus of an anesthetized Sprague-Dawley rat. Positive controls included animals injected with kainic acid, picrotoxin, or bicuculline. Seizures were recorded after injection of extracts from 6 out of 6 early stage granulomas, but only 1 out of 9 late stage granulomas. Injections of buffered saline, extracts from non-stimulated mouse spleen cells, and homogenates of viable parasite material caused no epileptiform activity. The data suggest that a substance in the granulomas early in the inflammatory response to the dying parasite is capable of inducing seizure activity. Further experiments are needed to dissect out the exact seizure mediator in the granuloma extracts.

Animals↗

Taenia crassiceps: androgen reconstitution of the host leads to protection during cysticercosis.

The effects of testosterone, dihydrotestosterone, and 17beta-estradiol in castrated mice of both sexes infected with Taenia crassiceps cysticerci were studied. The results showed that castration and treatment with either testosterone or dihydrotestosterone before infection decreased parasite loads by 50 and 70%, respectively, while the treatment with 17beta-estradiol increased it by three times in both genders, as compared with control mice. The specific splenocyte cell proliferation and IL-2 and IFN-gamma production were depressed in infected-castrated mice of both genders, while treatment with testosterone or dihydrotestosterone produced a significant proliferation recovery and enhanced production of IL-2 and IFN-gamma. On the other hand, the humoral response was unaffected with testosterone or dihydrotestosterone restitution, while the treatment with estradiol in both genders augmented the levels of anti-cysticerci IgG, as well as IL-6 and IL-10 production. These results suggest a protective role for androgens, possibly through the stimulation of the specific cellular immunity.

Animals↗

Vaccination against Taenia solium cysticercosis in pigs using native and recombinant oncosphere antigens.

Pigs were immunised with antigens derived from Taenia solium oncospheres or with a pool of three recombinant antigens from Taenia ovis, and subsequently challenged with T. solium eggs. The native oncosphere antigens induced 83% protection against viable, and 89% protection against the total number of cysticerci established following the challenge infection. Immunisation with the recombinant T. ovis antigens induced 93% protection against the establishment of viable cysticerci, and 74% protection against the total number of cysticerci. These results, and those achieved elsewhere with Taenia saginata and T. ovis, support the possibility of developing a practical vaccine to assist in the control of transmission of T. solium through pigs.

Animals↗

Cysticercosis of the fallopian tube: histology and microanalysis.

The authors identified a degenerated, focally calcified cestode larva (cysticercus) in the fallopian tube of a 50-year-old woman with endometriosis. The physiologic reaction to the larva was minimal, with some focal granulomatous salpingitis. No other focus of infection was detected. The differential diagnosis included trophoblastic tissue, foreign material, and parasites. Scanning electron microscopy and x-ray microanalysis of the organism revealed concentration of iodine in the subcuticular connective tissue of the larva and confirmed the calcium phosphate composition of the calcareous corpuscles. The presumed source of the iodine was the continued exposure of the larva to an environment rich in iodide secreted by the epithelium of the fallopian tube.

Cysticercosis↗

Hydatidosis and cysticercosis: the dynamics of transmission.

The infective pattern of taeniids in their intermediate hosts is determined by the complex interaction of parasite- and host-related factors. Many of these have been examined in this review, but particular emphasis has been placed on environmental factors that affect the free-living egg. While number, infectivity and distribution of eggs are among the important factors determining the infective pattern, the dynamics of this aspect of transmission have been previously neglected. The biotic potential of the large taeniid tapeworms is enormous. Eggs deposited on pasture are subjected to the microclimatic effects of the environment. They seem to tolerate a relatively wide temperature range. Heat down to -30 degrees C. However, they are rapidly killed by low humidity at all temperatures. Under more favourable conditions, they have finite life spans largely determined by the environmental temperature. At deposition, the egg population seems to be at various stages of maturity. Immature eggs appear to be able to mature under suitable environmental conditions and to become infective. They then age, and their infectivity to the intermediate host declines. At the population level, the changes in infectivity with time are determined by the relative stages of maturity within the egg population and the temperatures that it experiences. Under certain circumstances the infectivity of a given population may increase temporarily. The movements and defaecation habits of the definitive host determine the primary site of egg deposition. However, evidence is accumulating that considerable dispersion occurs almost immediately afterwards. Eggs have been shown to disperse up to 80 m within 10 days and there are indications that small numbers travel much further. Intermediate hosts, such as cattle and sheep, generally avoid grazing areas contaminated with faeces. Thus, dispersal enhances the chance of the eggs being ingested. The combination of high biotic potential and long-range dispersal means that individual infected definitive hosts can be responsible for infecting intermediate hosts over a very wide area. Although various possible agents have been suggested, the mechanisms responsible for disseminating eggs are still uncertain.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗