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1.
Pediatr Infect Dis J ; 36(5): 504-506, 2017 May.
Artigo em Inglês | MEDLINE | ID: mdl-28403054

RESUMO

A prospective cohort study of children with primary immunodeficiencies undergoing hematopoietic stem cell transplant in the United Kingdom investigated the extent and significance of Cryptosporidium carriage in this high risk group. Three of 42 children recruited were infected with Cryptosporidium, a lower proportion than previously described. One had serious disease. The underlying immunodeficiency likely had a bearing on the clinical presentation and possible outcome of infection.


Assuntos
Criptosporidiose/epidemiologia , Cryptosporidium/isolamento & purificação , Transplante de Células-Tronco Hematopoéticas , Síndromes de Imunodeficiência/epidemiologia , Criança , Pré-Escolar , Criptosporidiose/imunologia , Criptosporidiose/parasitologia , Criptosporidiose/terapia , Cryptosporidium/crescimento & desenvolvimento , Europa (Continente)/epidemiologia , Feminino , Humanos , Síndromes de Imunodeficiência/imunologia , Síndromes de Imunodeficiência/parasitologia , Síndromes de Imunodeficiência/terapia , Lactente , Masculino , Prevalência , Estudos Prospectivos
2.
Rev Med Interne ; 38(5): 337-339, 2017 May.
Artigo em Francês | MEDLINE | ID: mdl-28347510

RESUMO

INTRODUCTION: Good syndrome is a rare condition in which thymoma is associated with hypogammaglobulinemia. It is characterized by an increased susceptibility to infections. CASE REPORT: We report a woman with Good's syndrome diagnosed after severe congenital toxoplasmosis in her daughter, even though she was immunized against this infection during pregnancy. CONCLUSION: This presentation is very unusual by its early diagnosis and to our knowledge is the first report of parasitic infection in this syndrome.


Assuntos
Síndromes de Imunodeficiência/complicações , Complicações Parasitárias na Gravidez/etiologia , Timoma/complicações , Neoplasias do Timo/complicações , Toxoplasma/fisiologia , Toxoplasmose Congênita/etiologia , Toxoplasmose/transmissão , Adulto , Feminino , Humanos , Síndromes de Imunodeficiência/parasitologia , Recém-Nascido , Gravidez , Complicações Parasitárias na Gravidez/imunologia , Doenças Raras , Índice de Gravidade de Doença , Timoma/imunologia , Timoma/parasitologia , Neoplasias do Timo/imunologia , Neoplasias do Timo/parasitologia , Toxoplasma/imunologia , Toxoplasmose/complicações , Toxoplasmose/imunologia , Toxoplasmose Congênita/imunologia , Vacinação
3.
J Exp Med ; 213(7): 1307-18, 2016 06 27.
Artigo em Inglês | MEDLINE | ID: mdl-27270894

RESUMO

Human babesiosis is a tick-borne multisystem disease caused by Babesia species of the apicomplexan phylum. Most clinical cases and fatalities of babesiosis are caused by Babesia microti Current treatment for human babesiosis consists of two drug combinations, atovaquone + azithromycin or quinine + clindamycin. These treatments are associated with adverse side effects and a significant rate of drug failure. Here, we provide evidence for radical cure of experimental babesiosis in immunodeficient mice using a combination of an endochin-like quinolone (ELQ) prodrug and atovaquone. In vivo efficacy studies in mice using ELQ-271, ELQ-316, and the ELQ-316 prodrug, ELQ-334, demonstrated excellent growth inhibitory activity against the parasite, with potency equal to that of orally administered atovaquone at 10 mg/kg. Analysis of recrudescent parasites after ELQ or atovaquone monotherapy identified genetic substitutions in the Qi or Qo sites, respectively, of the cytochrome bc1 complex. Impressively, a combination of ELQ-334 and atovaquone, at doses as low as 5.0 mg/kg each, resulted in complete clearance of the parasite with no recrudescence up to 122 d after discontinuation of therapy. These results will set the stage for future clinical evaluation of ELQ and atovaquone combination therapy for treatment of human babesiosis.


Assuntos
Atovaquona/farmacologia , Babesia microti/imunologia , Babesiose/tratamento farmacológico , Síndromes de Imunodeficiência/parasitologia , Pró-Fármacos/farmacologia , Quinolonas/farmacologia , Animais , Babesiose/genética , Babesiose/imunologia , Síndromes de Imunodeficiência/genética , Síndromes de Imunodeficiência/imunologia , Camundongos , Camundongos SCID
4.
Eur J Immunol ; 32(3): 858-67, 2002 03.
Artigo em Inglês | MEDLINE | ID: mdl-11870630

RESUMO

In humans infected with lymphatic filariasis, microfilaraemia [the presence of microfilariae (Mf) in the blood] is generally associated with both poor antigen (Ag)-specific proliferative responses and with protection from severe disease. Clonal deletion has been suggested as one possible mechanism by which parasite-reactive lymphocytes, that may be capable of mediating resistance and/or immunopathology, are silenced in asymptomatic carriers. In this study we demonstrate that splenic lymphocytes from mice infected with microfilariae of Brugia pahangi display an Ag-specific proliferative defect. However, these cells were not completely unresponsive since they produced high levels of Ag-specific IFN-gamma. Using TdT-mediated dUTP-biotin nick end labeling for flow cytometry, CD4(+) lymphocytes from Mf-infected mice cultured with Ag showed high levels of apoptosis when compared to those from L3-infected mice which proliferated well in response to Ag. Treatment of Ag-stimulated cultures with aminoguanidine (AMG), an inhibitor of inducible nitric oxide synthase, rescued the CD4(+) T cells from apoptosis and reversed the proliferative defect. Furthermore, carboxyfluorescein diacetate succinimidyl ester labeling allowed the visualization of dividing CD4(+) T cells in cultures from Mf-infected animals only in the presence of AMG. We hypothesize that CD4(+) T cells indirectly trigger their own apoptosis by secreting significant quantities of IFN-gamma resulting in the induction of high levels of nitric oxide, and the subsequent elimination of effector T cells. Our findings are the first direct evidence that infection with Brugia Mf can selectively induce lymphocyte apoptosis, a phenomenon that could contribute to the proliferative defect and parasite persistence associated with the microfilaraemic state in the infected human.


Assuntos
Apoptose , Brugia pahangi/fisiologia , Linfócitos T CD4-Positivos/patologia , Filariose/imunologia , Microfilárias/fisiologia , Aedes/parasitologia , Animais , Antígenos de Helmintos/imunologia , Brugia pahangi/crescimento & desenvolvimento , Linfócitos T CD4-Positivos/enzimologia , Linfócitos T CD4-Positivos/imunologia , Linfócitos T CD4-Positivos/metabolismo , Células Cultivadas/efeitos dos fármacos , Inibidores Enzimáticos/farmacologia , Filariose/patologia , Citometria de Fluxo , Fluoresceínas/análise , Corantes Fluorescentes/análise , Gerbillinae , Guanidinas/farmacologia , Síndromes de Imunodeficiência/etiologia , Síndromes de Imunodeficiência/parasitologia , Interferon gama/biossíntese , Camundongos , Camundongos Endogâmicos BALB C , Óxido Nítrico/fisiologia , Óxido Nítrico Sintase/antagonistas & inibidores , Óxido Nítrico Sintase/fisiologia , Óxido Nítrico Sintase Tipo II , Parasitemia/imunologia , Parasitemia/patologia , Baço/patologia , Succinimidas/análise , Células Th2/imunologia , Células Th2/metabolismo
5.
J Immunol ; 165(2): 969-77, 2000 Jul 15.
Artigo em Inglês | MEDLINE | ID: mdl-10878373

RESUMO

A model of Leishmania major infection in C57BL/6 mice has been established that combines two main features of natural transmission: low dose (100 metacyclic promastigotes) and inoculation into a dermal site (the ear dermis). The evolution of the dermal lesion could be dissociated into two distinct phases. The initial "silent" phase, lasting 4-5 wk, favored establishment of the peak load of parasites in the dermis in the absence of lesion formation or any overt histopathologic changes in the site. The second phase corresponds to the development of a lesion associated with an acute infiltration of neutrophils, macrophages, and eosinophils into the dermis and was coincident with the killing of parasites in the site. The onset of immunity/pathology was correlated with the appearance of cells staining for IL-12p40 and IFN-gamma in the epidermal compartment, and an expansion of T cells capable of producing IFN-gamma in the draining lymph node. Parasite growth was not enhanced over the first 4.5 wk in anti-CD4-treated mice, SCID mice, or C57BL/6 mice deficient in IL-12p40, IFN-gamma, CD40 ligand, or inducible NO synthase. These mice all failed to ultimately control infection in the site, but in some cases (anti-CD4 treated, IL-12p40-/-, CD40 ligand-/-, and SCID) high dermal parasite loads were associated with little or no pathology. These results extend to a natural infection model a role for Th1 cells in both acquired resistance and lesion formation, and document the remarkable avoidance of this response during a prolonged phase of parasite amplification in the skin.


Assuntos
Leishmania major/crescimento & desenvolvimento , Leishmania major/imunologia , Leishmaniose Cutânea/imunologia , Leishmaniose Cutânea/parasitologia , Pele/imunologia , Pele/parasitologia , Animais , Células Cultivadas , Citocinas/biossíntese , Orelha Externa , Epiderme/imunologia , Epiderme/metabolismo , Epiderme/parasitologia , Epiderme/patologia , Imunidade Inata , Síndromes de Imunodeficiência/imunologia , Síndromes de Imunodeficiência/parasitologia , Síndromes de Imunodeficiência/patologia , Leishmania major/patogenicidade , Leishmaniose Cutânea/patologia , Leishmaniose Cutânea/transmissão , Linfonodos/imunologia , Linfonodos/metabolismo , Linfonodos/parasitologia , Linfonodos/patologia , Camundongos , Camundongos Endogâmicos C57BL , Camundongos Knockout , Camundongos SCID , Fatores de Tempo
6.
Wiad Parazytol ; 46(3): 335-44, 2000.
Artigo em Polonês | MEDLINE | ID: mdl-16883688

RESUMO

The congenital or acquired cause the state of immune deficiency. To acquired factors belong immunosuppressive therapy after grafting and in systemic diseases as infections with HIV. There is a number of parasitic organisms, mainly protozoa, which preferentially settle in immunocompromised persons. The opportunistic parasites are present in the nearest environment. Some of them were newly recognized as human invaders. The state of immune deficiency may reactivate latent infections, that occurs with Toxoplasma gondii infection. Some parasitic infections which are benign and self- resolving, when affecting immunocompetent hosts, become fulminant or disseminated and very often life - threatening in immunosuppressed individuals.


Assuntos
Síndromes de Imunodeficiência/epidemiologia , Síndromes de Imunodeficiência/parasitologia , Infecções Oportunistas/epidemiologia , Infecções Oportunistas/parasitologia , Doenças Parasitárias/epidemiologia , Doenças Parasitárias/parasitologia , Infecções Oportunistas Relacionadas com a AIDS/epidemiologia , Infecções Oportunistas Relacionadas com a AIDS/parasitologia , Infecções Oportunistas Relacionadas com a AIDS/prevenção & controle , Animais , Candidíase/epidemiologia , Candidíase/parasitologia , Candidíase/prevenção & controle , Causalidade , Comorbidade , Criptococose/epidemiologia , Criptococose/parasitologia , Criptococose/prevenção & controle , Infecções por Citomegalovirus/epidemiologia , Infecções por Citomegalovirus/parasitologia , Infecções por Citomegalovirus/prevenção & controle , Humanos , Hospedeiro Imunocomprometido/imunologia , Síndromes de Imunodeficiência/imunologia , Microsporidiose/epidemiologia , Microsporidiose/parasitologia , Microsporidiose/prevenção & controle , Infecções Oportunistas/prevenção & controle , Doenças Parasitárias/prevenção & controle , Pneumonia por Pneumocystis/epidemiologia , Pneumonia por Pneumocystis/parasitologia , Pneumonia por Pneumocystis/prevenção & controle , Infecções por Protozoários/epidemiologia , Infecções por Protozoários/parasitologia , Infecções por Protozoários/prevenção & controle
7.
Infect Immun ; 68(1): 170-5, 2000 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-10603384

RESUMO

We have studied immune mechanisms responsible for control of acute Giardia lamblia and Giardia muris infections in adult mice. Association of chronic G. lamblia infection with hypogammaglobulinemia and experimental infections of mice with G. muris have led to the hypothesis that antibodies are required to control these infections. We directly tested this hypothesis by infecting B-cell-deficient mice with either G. lamblia or G. muris. Both wild-type mice and B-cell-deficient mice eliminated the vast majority of parasites between 1 and 2 weeks postinfection with G. lamblia. G. muris was also eliminated in both wild-type and B-cell-deficient mice. In contrast, T-cell-deficient and scid mice failed to control G. lamblia infections, as has been shown previously for G. muris. Treatment of wild-type or B-cell-deficient mice with antibodies to CD4 also prevented elimination of G. lamblia, confirming a role for T cells in controlling infections. By infecting mice deficient in either alphabeta- or gammadelta-T-cell receptor (TCR)-expressing T cells, we show that the alphabeta-TCR-expressing T cells are required to control parasites but that the gammadelta-TCR-expressing T cells are not. Finally, infections in mice deficient in production of gamma interferon or interleukin 4 (IL-4) and mice deficient in responding to IL-4 and IL-13 revealed that neither the Th1 nor the Th2 subset is absolutely required for protection from G. lamblia. We conclude that a T-cell-dependent mechanism is essential for controlling acute Giardia infections and that this mechanism is independent of antibody and B cells.


Assuntos
Giardia lamblia/imunologia , Giardíase/imunologia , Linfócitos T/imunologia , Doença Aguda , Animais , Anticorpos/administração & dosagem , Linfócitos B/imunologia , Antígenos CD4/imunologia , Giardia lamblia/isolamento & purificação , Giardíase/parasitologia , Síndromes de Imunodeficiência/genética , Síndromes de Imunodeficiência/imunologia , Síndromes de Imunodeficiência/parasitologia , Interferon gama/deficiência , Interferon gama/genética , Interleucina-13/farmacologia , Interleucina-4/deficiência , Interleucina-4/genética , Interleucina-4/farmacologia , Camundongos , Camundongos Endogâmicos BALB C , Camundongos Endogâmicos C57BL , Camundongos Knockout , Camundongos SCID , Receptores de Antígenos de Linfócitos T alfa-beta/deficiência , Receptores de Antígenos de Linfócitos T alfa-beta/genética , Receptores de Antígenos de Linfócitos T gama-delta/deficiência , Receptores de Antígenos de Linfócitos T gama-delta/genética , Células Th1/imunologia , Células Th2/imunologia
8.
Med Trop (Mars) ; 59(1): 79-94, 1999.
Artigo em Francês | MEDLINE | ID: mdl-10472588

RESUMO

Cardiac, neurologic, and gastrointestinal manifestations of Chagas Disease have been well documented, but underlying pathophysiologic mechanisms, especially of chronic myocarditis, remain unclear. In the last decades, vectorial and transfusional transmission has been diminished. However congenital forms, which were long unknown and are still poorly understood, and reactive forms, which occur in patients with acquired or induced immunodeficiency, have confounded conventional wisdom concerning the evolution of this disease. Several new diagnostic tools have been developed without replacing the traditional methods, e.g. the xenodiagnostic technique proposed by Brumpt. With regard to indirect diagnosis, further progress is needed to improve specificity and sensitivity as well as the discriminating ability of the numerous techniques now available. Recently several double-blind randomized trials showed that benznidazole may be useful for early stage disease in children under 12 years of age. Further study with long-term follow-up will be necessary to determine the value of generalizing treatment to all patients with Chagas disease regardless of age and disease stage. However the ideal trypanocidal agent has yet to be found. Although attempts to immunize animals have not been complete failures, current results are not adequate to hold forth hope of a vaccine for use in man within the foreseeable future.


Assuntos
Doença de Chagas/fisiopatologia , Encefalopatias/parasitologia , Encefalopatias/fisiopatologia , Cardiomiopatia Chagásica/fisiopatologia , Doença de Chagas/congênito , Doença de Chagas/diagnóstico , Doença de Chagas/tratamento farmacológico , Doença de Chagas/transmissão , Criança , Pré-Escolar , Diagnóstico Diferencial , Vetores de Doenças , Método Duplo-Cego , Seguimentos , Gastroenteropatias/parasitologia , Gastroenteropatias/fisiopatologia , Humanos , Imunização , Síndromes de Imunodeficiência/parasitologia , Estudos Longitudinais , Miocardite/parasitologia , Miocardite/fisiopatologia , Nitroimidazóis/uso terapêutico , Ensaios Clínicos Controlados Aleatórios como Assunto , Sensibilidade e Especificidade , Tripanossomicidas/uso terapêutico , Vacinas
10.
J Immunol ; 163(2): 875-83, 1999 Jul 15.
Artigo em Inglês | MEDLINE | ID: mdl-10395682

RESUMO

Bruton's tyrosine kinase (Btk) mutant CBA/N mice show delayed clearance of injected microfilaria (mf) compared with wild-type CBA/J mice. Anti-mf T cells from CBA/N mice make relatively more IFN-gamma than those from CBA/J mice. The anti-mf T cell proliferative responses are also greater in CBA/N mice. This CBA/N immune phenotype is not restricted to filarial Ags, because immunization with pure proteins also yields T cell responses of greater proliferative magnitude skewed away from Th2 cytokines in CBA/N compared with CBA/J mice. The increased magnitude of CBA/N T cell proliferative responses is reflected in increases in both precursor frequencies and clonal burst sizes of responding Ag-specific T cells, and is independent of the source of re-stimulating APCs. Transfer of CBA/J peritoneal resident cells (PRCs) into CBA/N mice before pure protein immunization leads to a wild-type immune phenotype in the recipient CBA/N mice, with a reduction in the proliferative response and a relative decrease in the IFN-gamma produced. When wild-type PRC subpopulations are similarly transferred, the wild-type immune phenotype is transferred by macrophages rather than by B cells. Transfer of wild-type PRCs into CBA/N mice before injection of mf also causes similar changes in the anti-mf T cell responses and enhances the clearance of mf. Thus, Btk is involved in critical macrophage APC functions regulating priming of T cells, and can modulate these responses in pathophysiologically relevant fashion in vivo.


Assuntos
Células Apresentadoras de Antígenos/imunologia , Síndromes de Imunodeficiência/imunologia , Macrófagos Peritoneais/imunologia , Setaríase/imunologia , Setaríase/parasitologia , Células Th1/imunologia , Tirosina Quinase da Agamaglobulinemia , Animais , Anticorpos Anti-Helmínticos/biossíntese , Apresentação de Antígeno , Células Apresentadoras de Antígenos/parasitologia , Feminino , Síndromes de Imunodeficiência/genética , Síndromes de Imunodeficiência/parasitologia , Interferon gama/biossíntese , Ativação Linfocitária/genética , Macrófagos Peritoneais/parasitologia , Camundongos , Camundongos Endogâmicos CBA , Camundongos Mutantes , Microfilárias/crescimento & desenvolvimento , Microfilárias/imunologia , Proteínas Tirosina Quinases/genética , Soroalbumina Bovina/imunologia , Especificidade da Espécie , Células Th1/metabolismo , Fatores de Tempo
11.
J Immunol ; 162(11): 6690-700, 1999 Jun 01.
Artigo em Inglês | MEDLINE | ID: mdl-10352287

RESUMO

Cell-mediated immunity that results in IL-12/IFN-gamma production is essential to control infections by intracellular organisms. Studies in animal models revealed contrasting results in regard to the importance of CD40-CD40 ligand (CD40L) signaling for induction of a type 1 cytokine response against these pathogens. We demonstrate that CD40-CD40L interaction in humans is critical for generation of the IL-12/IFN-gamma immune response against Toxoplasma gondii. Infection of monocytes with T. gondii resulted in up-regulation of CD40. CD40-CD40L signaling was required for optimal T cell production of IFN-gamma in response to T. gondii. Moreover, patients with hyper IgM (HIGM) syndrome exhibited a defect in IFN-gamma secretion in response to the parasite and evidence compatible with impaired in vivo T cell priming after T. gondii infection. Not only was IL-12 production in response to T. gondii dependent on CD40-CD40L signaling, but also, patients with HIGM syndrome exhibited deficient in vitro secretion of this cytokine in response to the parasite. Finally, in vitro incubation with agonistic soluble CD40L trimer enhanced T. gondii-triggered production of IFN-gamma and, through induction of IL-12 secretion, corrected the defect in IFN-gamma production observed in HIGM patients. Our results are likely to explain the susceptibility of patients with HIGM syndrome to infections by opportunistic pathogens.


Assuntos
Antígenos CD40/metabolismo , Hipergamaglobulinemia/imunologia , Imunoglobulina M/biossíntese , Síndromes de Imunodeficiência/imunologia , Glicoproteínas de Membrana/sangue , Células Th1/imunologia , Toxoplasma/imunologia , Adjuvantes Imunológicos/fisiologia , Animais , Anticorpos Monoclonais/farmacologia , Anticorpos Antiprotozoários/sangue , Antígenos CD40/biossíntese , Antígenos CD40/imunologia , Ligante de CD40 , Células Cultivadas , Doença Crônica , Humanos , Hipergamaglobulinemia/parasitologia , Imunidade Celular , Síndromes de Imunodeficiência/parasitologia , Interferon gama/antagonistas & inibidores , Interferon gama/biossíntese , Interleucina-12/biossíntese , Interleucina-12/metabolismo , Ligantes , Ativação Linfocitária , Glicoproteínas de Membrana/agonistas , Glicoproteínas de Membrana/imunologia , Monócitos/imunologia , Monócitos/metabolismo , Transdução de Sinais/imunologia , Células Th1/metabolismo , Células Th1/parasitologia , Toxoplasmose/sangue , Toxoplasmose/imunologia , Regulação para Cima/imunologia
12.
J Infect Dis ; 173(4): 1041-3, 1996 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-8603949

RESUMO

To establish models for studying recurrence of visceral leishmaniasis, a growing problem in T cell-deficient patients, two approaches were investigated: treatment of euthymic BALB/c mice with quiescent Leishmania donovani infection with T cell-depleting or anti-cytokine antibodies and serial observation of acutely infected nude BALB/c mice after an initial antileishmanial response induced by amphotericin B treatment. In chronically infected euthymic mice, maintenance of acquired immunity and prevention of relapse required CD4 cells and a multicytokine-dependent mechanism involving endogenous interleukin-2, interferon-gamma, and tumor necrosis factor-alpha. Acutely infected nude mice responded to amphotericin B with a > or = 85% reduction in liver parasite burdens; however, after a brief lag, visceral infection readily recurred in the posttreatment period. Both models may be useful for testing experimental interventions designed to reduce relapse of previously controlled visceral leishmaniasis in T cell-deficient hosts.


Assuntos
Leishmania donovani/patogenicidade , Leishmaniose Visceral/imunologia , Animais , Doença Crônica , Modelos Animais de Doenças , Síndromes de Imunodeficiência/parasitologia , Depleção Linfocítica , Camundongos , Camundongos Endogâmicos BALB C , Camundongos Nus , Linfócitos T/imunologia , Fatores de Tempo
13.
Pediatr Infect Dis J ; 14(12): 1042-7, 1995 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-8745015

RESUMO

Little information is available on asymptomatic carriage of Cryptosporidium in immunocompetent and immunodeficient children. We prospectively studied a group of asymptomatic children, 78 immunocompetent and 50 immunodeficient, to document the incidence of asymptomatic carriage of cryptosporidiosis in such a population. We also investigated whether the treatment of children who carried asymptomatic cryptosporidiosis could help in reducing their risk of gastrointestinal symptoms as well as the shedding of infectious oocysts. The occurrence of multiple infections with common intestinal pathogens including Giardia lamblia was also investigated. Asymptomatic cryptosporidiosis was documented in 6.4% of immunocompetent and 22% of immunodeficient children. In a control symptomatic population Cryptosporidium was found in 4.4% of immunocompetent and 4.8% of immunodeficient children. Asymptomatic carriage of Cryptosporidium was documented in 2 human immunodeficiency virus-infected children, one of whom also carried Giardia asymptomatically. Treatment with spiramycin (100 mg/kg daily for 14 days) reduced significantly the duration of the shedding of potentially infectious oocysts. Finally no gastrointestinal symptoms developed in children treated for asymptomatic infection with Cryptosporidium, whereas children who were not treated developed gastrointestinal symptoms.


Assuntos
Portador Sadio/parasitologia , Criptosporidiose/etiologia , Cryptosporidium/isolamento & purificação , Fezes/parasitologia , Giardia lamblia/isolamento & purificação , Imunocompetência , Síndromes de Imunodeficiência/parasitologia , Adolescente , Animais , Antibacterianos/uso terapêutico , Portador Sadio/tratamento farmacológico , Criança , Pré-Escolar , Criptosporidiose/tratamento farmacológico , Humanos , Síndromes de Imunodeficiência/tratamento farmacológico , Lactente , Estudos Prospectivos , Espiramicina/uso terapêutico
14.
Radiol Med ; 87(5 Suppl 2): 13-25, 1994 May.
Artigo em Italiano | MEDLINE | ID: mdl-8209022

RESUMO

Just like the lung, the brain and the spinal cord are target organs for opportunistic infections and tumors in immunocompromised patients. HIV infections and AIDS-related conditions represent the most common cause of immunodeficiency: other causes are hemoproliferative disorders and organ transplantation, but especially long-term drug and radiation therapies. Neurologic (focal, diffuse, meningeal or spinal) signs are the results of CNS infections and/or tumors or of treatment complications. Neuroimaging techniques (MRI better than CT) allow the infective or neoplastic causes of neurologic complications to be nearly always recognized and are therefore major tools for diagnosis and treatment. Lesions characterization is more difficult, since CT and MR patterns are definitely more affected by the evolutive phases of the lesions (encephalitis, cerebritis, abscess) and by their sites than by specific infective agents. However, the knowledge of the statistical possibility of brain and spine infections according to the type of immunocompromission is useful in many cases.


Assuntos
Doenças do Sistema Nervoso Central/diagnóstico por imagem , Infecções por HIV/complicações , Hospedeiro Imunocomprometido , Síndromes de Imunodeficiência/diagnóstico por imagem , Doenças do Sistema Nervoso Central/microbiologia , Doenças do Sistema Nervoso Central/parasitologia , Infecções por HIV/diagnóstico por imagem , Humanos , Síndromes de Imunodeficiência/microbiologia , Síndromes de Imunodeficiência/parasitologia , Tomografia Computadorizada por Raios X
15.
Antimicrob Agents Chemother ; 38(4): 865-7, 1994 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-8031061

RESUMO

Lasalocid, sinefungin, and dehydroepiandrosterone were tested for anticryptosporidial activity with an immunodeficient mouse model at doses that have been reported effective when tested with immunosuppressed rodent models. Small but significant reductions in oocyst excretion were only observed under some conditions with lasalocid and dehydroepiandrosterone, but sinefungin had no effect.


Assuntos
Coccidiostáticos/uso terapêutico , Criptosporidiose/tratamento farmacológico , Cryptosporidium parvum/efeitos dos fármacos , Síndromes de Imunodeficiência/parasitologia , Adenosina/análogos & derivados , Adenosina/uso terapêutico , Animais , Antiprotozoários/uso terapêutico , Criptosporidiose/parasitologia , Desidroepiandrosterona/uso terapêutico , Lasalocida/uso terapêutico , Masculino , Camundongos , Camundongos Nus , Esplenectomia
17.
Nature ; 356(6367): 338-40, 1992 Mar 26.
Artigo em Inglês | MEDLINE | ID: mdl-1549177

RESUMO

The beta 2-microglobulin (beta 2m) protein associates with the products of the class I major histocompatibility (MHC) loci; this combination functions in the thymic development of and antigen presentation to CD8+ T cells. Mice in which the beta 2m gene has been disrupted by homologous recombination fail to express class I MHC gene products, and therefore lack CD8+ T cells and measurable cytotoxic T-cell responses. However, beta 2m- mice appear to have normal development of both CD4+ alpha/beta T-cell receptor (TCR+) and gamma/delta TCR+ T cells and are not overtly more susceptible than beta 2m+ mice to potential environmental agents of infection or to experimental viral infection. Here we show that beta 2m- mice suffer high parasitaemias and early death when infected with the obligate cytoplasmic protozoan parasite Trypanosoma cruzi. Despite this increased susceptibility, the beta 2m- mice are more responsive than their beta 2m+ littermates in terms of lymphokine production, making higher levels of both interleukin-2 and interferon-gamma in response to mitogen stimulation. In addition, the beta 2m- mice show essentially no inflammatory response in parasite-infected tissues. These results confirm previous experiments on mice depleted of CD8+ cells using antibody treatment in demonstrating the importance of CD8+ T cells in immune protection in T. cruzi infection. They also implicate CD8+ T cells and/or class I MHC molecules in regulation of lymphokine production and recruitment of inflammatory cells.


Assuntos
Doença de Chagas/imunologia , Síndromes de Imunodeficiência/parasitologia , Subpopulações de Linfócitos T/imunologia , Microglobulina beta-2/deficiência , Doença Aguda , Animais , Antígenos CD8/análise , Doença Crônica , Coração/parasitologia , Interferon gama/biossíntese , Interleucina-2/biossíntese , Músculos/parasitologia , Músculos/patologia , Miocárdio/patologia , Fatores de Tempo , Trypanosoma cruzi/imunologia
18.
Int Immunol ; 3(5): 427-33, 1991 May.
Artigo em Inglês | MEDLINE | ID: mdl-1911532

RESUMO

Infection of several mouse strains with Trypanosoma cruzi stimulates high levels of T and B lymphocyte activities which persist during the chronic phase and is followed by specific immunosuppression and severe autoimmune pathology. Infected BALB.Xid mice carrying an X-linked mutation and lacking CD5 B cells, display poor B cell responses to T. cruzi infection, accompanied by low levels of specific and non-specific immunoglobulins in the serum. However, these animals control parasitemia, do not show the wasting observed in BALB/c mice, and develop almost no pathology early in the chronic phase. The infection of (BALB.Xid female x BALB/c male) F1 animals shows that immunodefective males behave like Xid animals in contrast to females which respond as normal BALB/c mice. These results indicate that the Xid locus controls lymphocyte responses, parasite clearance and pathology in experimental Chagas' disease.


Assuntos
Doença de Chagas/imunologia , Síndromes de Imunodeficiência/parasitologia , Camundongos Mutantes/parasitologia , Trypanosoma cruzi/isolamento & purificação , Animais , Anticorpos Antiprotozoários/biossíntese , Doenças Autoimunes/genética , Doenças Autoimunes/imunologia , Linfócitos B/imunologia , Linfócitos B/patologia , Cardiomiopatia Chagásica/imunologia , Doença de Chagas/complicações , Doença de Chagas/genética , Doença Crônica , Feminino , Imunidade Inata/genética , Imunidade Inata/imunologia , Síndromes de Imunodeficiência/complicações , Síndromes de Imunodeficiência/genética , Ativação Linfocitária , Masculino , Camundongos , Camundongos Endogâmicos BALB C , Camundongos Mutantes/genética , Camundongos Mutantes/imunologia , Trypanosoma cruzi/imunologia
19.
Parassitologia ; 32(2): 275-81, 1990 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-2132438

RESUMO

In sera of 35 dogs with generalised leishmaniasis elevated levels of circulating immune complexes were detected by the 125I-C1q binding test. Furthermore, anti-heart muscle and anti-smooth muscle antibodies were detected by an indirect immunofluorescence technique in sera of infected dogs.


Assuntos
Complexo Antígeno-Anticorpo/sangue , Autoanticorpos/sangue , Doenças do Cão/imunologia , Leishmaniose Visceral/veterinária , Animais , Doenças Autoimunes/imunologia , Doenças Autoimunes/parasitologia , Doenças Autoimunes/veterinária , Cães/imunologia , Feminino , Síndromes de Imunodeficiência/imunologia , Síndromes de Imunodeficiência/parasitologia , Síndromes de Imunodeficiência/veterinária , Leishmaniose Visceral/complicações , Leishmaniose Visceral/imunologia , Masculino , Fagocitose
20.
Arch Roum Pathol Exp Microbiol ; 48(4): 357-65, 1989.
Artigo em Inglês | MEDLINE | ID: mdl-2485207

RESUMO

By using the elective diagnosis methodology for Cryptosporidium (modified Ziehl-Neelsen and Heine stainings), 481 faeces samples from patients--children and adults--presenting acute or prolonged gastroenteritis and also from asymptomatic ones, but with professional, immunological or pharmacological risk for infection, were studied. Twelve Cryptosporidium positive cases were identified, meaning a general prevalence of 2.48% Cryptosporidium infection was detected in all investigated epidemiological groups: children, animal handlers, immunodeficient patients, immunocompetent adults with acute gastroenteritis. The risk factors hierarchy elicited the role of children collectivities attending, for acquiring the parasite in infantile cryptosporidiosis, while the opportunistic and zoonotic feature of the disease was especially present in adults' cryptosporidiosis. The assessment of cryptosporidiosis evolution, according to patients' immune status, has not allowed an obvious clinical discrepancy, since the immunocompetent subjects with professional risk had presented a prolonged oocysts excretion. The different clinico-epidemiological and parasitological features of Cryptosporidium infection are commented and the importance of applying Cryptosporidium methodology in current diagnosis practice is emphasized.


Assuntos
Criptosporidiose/parasitologia , Adulto , Animais , Criança , Criptosporidiose/epidemiologia , Criptosporidiose/imunologia , Cryptosporidium/isolamento & purificação , Fezes/parasitologia , Humanos , Imunocompetência/imunologia , Síndromes de Imunodeficiência/epidemiologia , Síndromes de Imunodeficiência/imunologia , Síndromes de Imunodeficiência/parasitologia , Prevalência , Fatores de Risco , Romênia/epidemiologia , Coloração e Rotulagem/métodos
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