The Experts below are selected from a list of 1035 Experts worldwide ranked by ideXlab platform
Mahendra Bhandari - One of the best experts on this subject based on the ideXlab platform.
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Visceral Leishmaniasis in a Renal Transplant Recipient: Diagnostic and Therapeutic Problems
American journal of nephrology, 1996Co-Authors: Raj K. Sharma, Ratan Jha, Pradeep Kumar, Vijay Kher, Amit Gupta, Anant Kumar, Sanjeev Gulati, Pradeep Arora, Manjula Murari, Mahendra BhandariAbstract:Visceral leishmaniasis is infrequently reported in renal transplant recipients. A 40-year-old renal transplant recipient developed hepatosplenomegaly and pyrexia of unknown origin 5 months after transplantation. Visceral leishmaniasis was confirmed on bone marrow examination. The usual dose of Antiparasitic Therapy with stibogluconate sodium failed to eradicate Leishmania donovani. High-dose conventional Therapy with stibogluconate sodium for an extended period of time was successful in the treatment of a relapse of leishmaniasis.
Brian G. Blackburn - One of the best experts on this subject based on the ideXlab platform.
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SYMPOSIUM ON ANTIMICROBIAL TherapyAntiparasitic Therapy
Mayo Clinic proceedings, 2011Co-Authors: Shanthi Kappagoda, Upinder Singh, Brian G. BlackburnAbstract:Parasitic diseases affect more than 2 billion people globally and cause substantial morbidity and mortality, particularly among the world's poorest people. This overview focuses on the treatment of the major protozoan and helminth infections in humans. Recent developments in Antiparasitic Therapy include the expansion of artemisinin-based therapies for malaria, new drugs for soil-transmitted helminths and intestinal protozoa, expansion of the indications for Antiparasitic drug treatment in patients with Chagas disease, and the use of combination Therapy for leishmaniasis and human African trypanosomiasis.
Tomasz Kula - One of the best experts on this subject based on the ideXlab platform.
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Endobiont Viruses Sensed by the Human Host – Beyond Conventional Antiparasitic Therapy
PloS one, 2012Co-Authors: Raina N. Fichorova, Yujin Lee, Hidemi S. Yamamoto, Yuko Takagi, Gary R. Hayes, Russell P. Goodman, Xenia Chepa-lotrea, Olivia R. Buck, Richard Murray, Tomasz KulaAbstract:Wide-spread protozoan parasites carry endosymbiotic dsRNA viruses with uncharted implications to the human host. Among them, Trichomonas vaginalis, a parasite adapted to the human genitourinary tract, infects globally ∼250 million each year rendering them more susceptible to devastating pregnancy complications (especially preterm birth), HIV infection and HPV-related cancer. While first-line antibiotic treatment (metronidazole) commonly kills the protozoan pathogen, it fails to improve reproductive outcome. We show that endosymbiotic Trichomonasvirus, highly prevalent in T. vaginalis clinical isolates, is sensed by the human epithelial cells via Toll-like receptor 3, triggering Interferon Regulating Factor -3, interferon type I and proinflammatory cascades previously implicated in preterm birth and HIV-1 susceptibility. Metronidazole treatment amplified these proinflammatory responses. Thus, a new paradigm targeting the protozoan viruses along with the protozoan host may prevent trichomoniasis-attributable inflammatory sequelae.
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endobiont viruses sensed by the human host beyond conventional Antiparasitic Therapy
PLOS ONE, 2012Co-Authors: Raina N. Fichorova, Yujin Lee, Hidemi S. Yamamoto, Yuko Takagi, Gary R. Hayes, Russell P. Goodman, Olivia R. Buck, Xenia Chepalotrea, Ryan Murray, Tomasz KulaAbstract:Wide-spread protozoan parasites carry endosymbiotic dsRNA viruses with uncharted implications to the human host. Among them, Trichomonas vaginalis, a parasite adapted to the human genitourinary tract, infects globally ∼250 million each year rendering them more susceptible to devastating pregnancy complications (especially preterm birth), HIV infection and HPV-related cancer. While first-line antibiotic treatment (metronidazole) commonly kills the protozoan pathogen, it fails to improve reproductive outcome. We show that endosymbiotic Trichomonasvirus, highly prevalent in T. vaginalis clinical isolates, is sensed by the human epithelial cells via Toll-like receptor 3, triggering Interferon Regulating Factor -3, interferon type I and proinflammatory cascades previously implicated in preterm birth and HIV-1 susceptibility. Metronidazole treatment amplified these proinflammatory responses. Thus, a new paradigm targeting the protozoan viruses along with the protozoan host may prevent trichomoniasis-attributable inflammatory sequelae.
Raj K. Sharma - One of the best experts on this subject based on the ideXlab platform.
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Visceral Leishmaniasis in a Renal Transplant Recipient: Diagnostic and Therapeutic Problems
American journal of nephrology, 1996Co-Authors: Raj K. Sharma, Ratan Jha, Pradeep Kumar, Vijay Kher, Amit Gupta, Anant Kumar, Sanjeev Gulati, Pradeep Arora, Manjula Murari, Mahendra BhandariAbstract:Visceral leishmaniasis is infrequently reported in renal transplant recipients. A 40-year-old renal transplant recipient developed hepatosplenomegaly and pyrexia of unknown origin 5 months after transplantation. Visceral leishmaniasis was confirmed on bone marrow examination. The usual dose of Antiparasitic Therapy with stibogluconate sodium failed to eradicate Leishmania donovani. High-dose conventional Therapy with stibogluconate sodium for an extended period of time was successful in the treatment of a relapse of leishmaniasis.
Hector H. Garcia - One of the best experts on this subject based on the ideXlab platform.
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efficacy of combined Antiparasitic Therapy with praziquantel and albendazole for neurocysticercosis a double blind randomised controlled trial
Lancet Infectious Diseases, 2014Co-Authors: Hector H. Garcia, Isidro Gonzales, Andres G Lescano, Javier A Bustos, Mirko Zimic, Diego Escalante, Herbert Saavedra, Martin Gavidia, Lourdes Rodriguez, Enrique NajarAbstract:Summary Background Neurocysticercosis causes a substantial burden of seizure disorders worldwide. Treatment with either praziquantel or albendazole has suboptimum efficacy. We aimed to establish whether combination of these drugs would increase cysticidal efficacy and whether complete cyst resolution results in fewer seizures. We added an increased dose albendazole group to establish a potential effect of increased albendazole concentrations. Methods In this double-blind, placebo-controlled, phase 3 trial, patients with viable intraparenchymal neurocysticercosis were randomly assigned to receive 10 days of combined albendazole (15 mg/kg per day) plus praziquantel (50 mg/kg per day), standard albendazole (15 mg/kg per day), or increased dose albendazole (22·5 mg/kg per day). Randomisation was done with a computer generated schedule balanced within four strata based on number of cysts and concomitant antiepileptic drug. Patients and investigators were masked to group assignment. The primary outcome was complete cyst resolution on 6-month MRI. Enrolment was stopped after interim analysis because of parasiticidal superiority of one treatment group. Analysis excluded patients lost to follow-up before the 6-month MRI. This trial is registered with ClinicalTrials.gov, number NCT00441285. Findings Between March 3, 2010 and Nov 14, 2011, 124 patients were randomly assigned to study groups (41 to receive combined albendazole plus praziquantel [39 analysed], 43 standard albendazole [41 analysed], and 40 increased albendazole [38 analysed]). 25 (64%) of 39 patients in the combined treatment group had complete resolution of brain cysts compared with 15 (37%) of 41 patients in the standard albendazole group (rate ratio [RR] 1·75, 95% CI 1·10–2·79, p=0·014). 20 (53%) of 38 patients in the increased albendazole group had complete cyst resolution at 6-month MRI compared with 15 (37%) of 41 patients in the standard albendazole group (RR 1·44, 95% CI 0·87–2·38, p=0·151). No significant differences in adverse events were reported between treatment groups (18 in combined treatment group, 11 in standard albendazole group, and 19 in increased albendazole group). Interpretation Combination of albendazole plus praziquantel increases the parasiticidal effect in patients with multiple brain cysticercosis cysts without increased side-effects. A more efficacious parasiticidal regime without increased treatment-associated side-effects should improve the treatment and long term prognosis of patients with neurocysticercosis. Funding National Institute of Neurological Disorders and Stroke (NINDS), National Institutes of Health.
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Mechanisms Regulating Monocyte CXCL8 Secretion in Neurocysticercosis and the Effect of Antiparasitic Therapy
Journal of immunology (Baltimore Md. : 1950), 2010Co-Authors: Jasim Uddin, Hector H. Garcia, Armando E. Gonzalez, Robert H. Gilman, Silvia Rodriguez, Lynette H. Thomas, Carlton A. Evans, Daniel G. Remick, Jon S. FriedlandAbstract:Neurocysticercosis (NCC) due to infection with Taenia solium is a major cause of epilepsy worldwide. Larval degeneration, which may follow Antiparasitic treatment, results in clinical symptoms due to inflammatory cell influx. Mechanisms regulating this are not well understood, but chemokines have a key role. Stimulation of human monocytes by cyst Ags from NCC-infected pigs showed that scolex and membrane Ags drive CXCL8 and CCL2 secretion. Antiparasitic treatment of pigs increased CXCL8 in response to brain, but not muscle, cyst Ags. Cyst-fluid Ags did not elicit monocyte chemokine secretion, inhibited LPS-induced CXCL8 by up to 89%, but did not alter CCL2 secretion. This effect was inhibited by anti–IL-10 Abs. Plasma CXCL8, TNF-α, IL-10, eotaxin, IL-1, IL-1ra, soluble IL-1R-II, and soluble TNFR-I and -II levels were evaluated in 167 NCC patients. Patients had lower plasma CXCL8 and TNF-α concentrations than control subjects. In summary, larval Ags from brain and muscle cysts differentially regulate chemokine secretion. Cyst-fluid inhibits CXCL8, and this is blocked by anti–IL-10 Abs. CXCL8 concentrations are decreased in patient plasma. Following anti-parasitic Therapy, scolex and membrane Ags are exposed, and cyst fluid is decreased, leading to inflammatory cell influx. Taken together, the cellular, porcine, and human data may explain, in part, why NCC is usually asymptomatic but may cause proinflammatory symptoms, particularly following treatment.
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Circulating parasite antigen in patients with hydrocephalus secondary to neurocysticercosis.
American Journal of Tropical Medicine and Hygiene, 2002Co-Authors: Hector H. Garcia, Armando E. Gonzalez, Robert H. Gilman, Teresa Bernal, Silvia Rodriguez, E. J. Pretell, O Azcurra, R. M E Parkhouse, Victor C. W. Tsang, Leslie J.s. HarrisonAbstract:End stages of neurocysticercosis include residual intraparenchymal brain calcifications and hydrocephalus. Although brain calcifications alone have a benign prognosis, hydrocephalus is frequently associated with chronic inflammation and intracranial hypertension, together with a protracted clinical evolution, and may lead to patient deaths. By using a monoclonal-based antigen detection enzyme-linked immunosorbent assay, we measured the levels of circulating parasite antigen in the sera of 56 patients with neurocysticercosis: 27 with calcifications only and 29 with hydrocephalus. The assay gave positive results in 14 of 29 patients with hydrocephalus but was consistently negative in patients with calcifications. Circulating parasite antigen in hydrocephalus secondary to neurocysticercosis indicates the presence of live parasites in these patients and thus a potential benefit from Antiparasitic Therapy.
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Serologic Evolution of Neurocysticercosis Patients after Antiparasitic Therapy
The Journal of infectious diseases, 1997Co-Authors: Hector H. Garcia, Armando E. Gonzalez, Robert H. Gilman, Manuel Catacora, Manuela Verastegui, Victor C. W. TsangAbstract:Neurocysticercosis is the main cause of acquired epilepsy in developing countries and is an emerging disease in the United States. Introduction of the immunoblot assay provided a new tool for the diagnosis and monitoring of neurocysticercosis. This study analyzed the relationship between clinical characteristics of cerebral infection (number and type of lesions) plus the baseline response on immunoblot and the changes observed after Therapy. Reaction to all 7 diagnostic bands was associated with severe infection (more lesions). Seventeen patients (35%) had no active lesions on computed tomography (CT) 3 months after Therapy and were considered cured. Although most cured patients remained seropositive after 1 year, 3 became seronegative before 9 months. In these 3 cases, the lesions had resolved on CT at 3 months. Persistent seropositivity does not necessarily indicate active infection. Serologic follow-up will be clinically helpful only in rare cases in which early antibody disappearance occurs.
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Medical Treatment of Cysticercosis: Ineffective vs Effective
Archives of neurology, 1995Co-Authors: Hector H. Garcia, Robert H. GilmanAbstract:In the section "Controversies in Neurology" of the January issue of theArchives, Kramer 1 and Del Brutto 2 do a commendable job of defending opposed positions about the role of Antiparasitic Therapy in the management of neurocysticercosis. We would like, however, to discuss the final statements of the section editor, Dr Hachinski, 3 that placebo-controlled therapeutic trials for neurocysticercosis are not plausible for ethical reasons. The actual knowledge of the evolution of untreated cysticercosis is scarce and based on anecdotal case reports. 4,5 Selection bias affects the validity of these reports: cases with more severe symptoms will be more likely to be chosen for study since patients with milder symptoms will be less likely to seek medical attention. "Historical" controls (patients who had computed tomographic studies performed before treatment) have also shown that lesions do not significantly increase in number or size. 6,7 These historical controls were selected from
