RESUMO
Leptospirosis has been investigated in several species of wild animals. The white-eared opossum (Didelphis albiventris) is a mammal common in the brazilian semi-arid, so, this study aimed to investigate its role in the occurrence of the leptospirosis in the region Northeast of Brazil. 12 animals were used, from which samples were collected for the attempt of isolation, molecular detection and serological examination. There was no microbial growth, nor were any anti-Leptospira sp. antibodies found in the serological samples. The PCR detected leptospiric DNA in the central nervous system (CNS) of five animals (41.7 %). The gene in one of the samples was sequenced and showed identity with Leptospira interrogans. The presence of Leptospira sp. in the CNS of Didelphis albiventris does not allow the characterization of the studied animals as reservoirs with potential for transmission of the pathogen in the region, however it represents a site that needs to be further investigated.
Assuntos
Portador Sadio/veterinária , Sistema Nervoso Central/parasitologia , Didelphis/parasitologia , Leptospira/classificação , Leptospirose/veterinária , Animais , Brasil/epidemiologia , Portador Sadio/epidemiologia , Portador Sadio/parasitologia , Leptospira/genética , Leptospira/isolamento & purificação , Leptospirose/epidemiologia , Leptospirose/parasitologia , Filogenia , Alinhamento de Sequência/veterináriaRESUMO
A doença de Chagas ainda é uma doença tropical muito prevalente no Brasil. Pode apresentar duas fases (aguda e crônica) e exibe grandes repercussões, sobretudo as que envolvem o sistema nervoso periférico e/ou central. Com o aumento do número de pessoas vivendo em estado (transitório ou permanente) de imunossupressão, os casos de manifestações neurológicas por neurochagas aumentaram, e este tornou-se um importante diagnóstico diferencial com outras doenças oportunistas. Este artigo teve como objetivo revisar os principais aspectos clínicos e terapêuticos da doença de Chagas no sistema nervoso central.
Chagas disease is still a very prevalent tropical disease in Brazil. It can have two phases - acute and chronic and shows major repercussions, especially those involving the peripheral and/ or central nervous system. With the increase in the number of people living in the (transient or permanent) state of immunosuppression the cases of neurological manifestations of Chagas disease increased and this became an important differential diagnosis with other opportunistic diseases. This article aimed to review the main clinical and therapeutic aspects of central nervous system Chagas disease
Assuntos
Humanos , Infecções por HIV/complicações , Sistema Nervoso Central/parasitologia , Sistema Nervoso Central/virologia , Doença de Chagas/complicações , Infecções por HIV/diagnóstico , Infecções por HIV/fisiopatologia , Infecções por HIV/imunologia , Sistema Nervoso Central/imunologia , Doença de Chagas/diagnóstico , Doença de Chagas/fisiopatologia , Doença de Chagas/imunologia , Doença de Chagas/tratamento farmacológico , Diagnóstico DiferencialRESUMO
Neurocysticercosis (NCC), caused by Taenia solium larvae that reside in the central nervous system, results in serious public health and medical issues in many regions of the world. Current diagnosis of NCC is complex requiring both serology and costly neuroimaging of parasitic cysts in the brain. This diagnostic pipeline can be problematic in resource-constrained settings. There is an unmet need for a highly sensitive and clinically informative diagnostic test to complement the present diagnostic approaches. Here, we report that T. solium-derived cell-free DNA is readily detectable in the urine of patients with the subarachnoid and parenchymal forms of NCC, and discuss the potential utility of this approach in enhancing and refining T. solium diagnostics.
Assuntos
Ácidos Nucleicos Livres/genética , Disfunção Cognitiva/parasitologia , DNA de Helmintos/genética , Neurocisticercose/parasitologia , Taenia solium/genética , Animais , Ácidos Nucleicos Livres/sangue , Ácidos Nucleicos Livres/urina , Sistema Nervoso Central/parasitologia , Sistema Nervoso Central/fisiopatologia , Disfunção Cognitiva/diagnóstico por imagem , Disfunção Cognitiva/fisiopatologia , DNA de Helmintos/sangue , DNA de Helmintos/urina , Humanos , Larva/genética , Neurocisticercose/diagnóstico por imagem , Neurocisticercose/fisiopatologia , Neuroimagem/métodos , Peru , Reação em Cadeia da Polimerase/métodos , Taenia solium/isolamento & purificaçãoRESUMO
The taeniasis/cysticercosis complex is a zoonosis caused by the presence of the parasite Taenia solium in humans. It is considered a neglected disease that causes serious public health and economic problems in developing countries. In humans, the most common locations for the larval form are the skeletal muscles, ocular system, and the central nervous system, which is the most clinically important. Several glycoproteins of T. solium and Taenia crassiceps cysticerci have been characterized and studied for their use in the immunodiagnosis of neurocysticercosis and/or the development of synthetic or recombinant vaccines against cysticercosis. The aim of this study was to perform a gel-free shotgun proteomic analysis to identify saline vesicular extract (SVE) proteins of T. solium and T. crassiceps cysticerci. After solubilization of the SVE with and without surfactant reagent and in-solution digestion, the proteins were analyzed by LC-MS/MS. Use of a surfactant resulted in a significantly higher number of proteins that were able to be identified by LC-MS/MS. Novel proteins were identified in T. solium and T. crassiceps SVE. The qualitative analysis revealed a total of 79 proteins in the Taenia species: 29 in T. solium alone, 11 in T. crassiceps alone, and 39 in both. These results are an important contribution to support future investigations and for establishing a Taenia proteomic profile to study candidate biomarkers involved in the diagnosis or pathogenesis of neurocysticercosis.
Assuntos
Extratos Celulares/análise , Cysticercus/metabolismo , Proteoma/análise , Proteínas de Protozoários/análise , Proteínas de Protozoários/imunologia , Taenia solium/metabolismo , Animais , Antígenos de Helmintos , Sistema Nervoso Central/parasitologia , Cromatografia Líquida , Cysticercus/genética , Cysticercus/imunologia , Países em Desenvolvimento , Perfilação da Expressão Gênica , Humanos , Larva/metabolismo , Músculo Esquelético/parasitologia , Doenças Negligenciadas/parasitologia , Neurocisticercose/diagnóstico , Neurocisticercose/parasitologia , Proteômica , Saúde Pública , Taenia solium/genética , Taenia solium/imunologia , Teníase/diagnóstico , Teníase/parasitologia , Zoonoses/parasitologiaRESUMO
BACKGROUND: Canine visceral leishmaniasis (CVL) is endemic in São Luís Maranhão/Brazil and it leads a varied clinical picture, including neurological signs. RESULTS: Histopathological evaluation showed that 14 dogs exhibited pathological alterations in at least one of the analyzed areas. Of these, mononuclear inflammatory reaction was the most frequent, although other lesions, such as hemorrhage, chromatolysis and gliosis were also observed. The presence of L. infantum amastigotes was confirmed in eight dogs, identified in four regions: telencephalon, hippocampus, thalamus and caudal colliculus, but only one presented neurological signs. Polymerase chain reaction results detected the DNA of the parasite in 11 samples from seven dogs. The positive areas were the telencephalon, thalamus, hippocampus, cerebellum, caudal and rostral colliculus. CONCLUSION: These results reveal that during canine visceral leishmaniasis, the central nervous system may display some alterations, without necessarily exhibiting clinical neurological manifestations. In addition, the L. infantum parasite has the ability to cross the blood brain barrier and penetrate the central nervous system.
Assuntos
Sistema Nervoso Central/parasitologia , Doenças do Cão/parasitologia , Leishmania infantum , Leishmaniose Visceral/veterinária , Animais , Sistema Nervoso Central/patologia , DNA de Protozoário/genética , Doenças do Cão/patologia , Cães , Feminino , Hipocampo/parasitologia , Hipocampo/patologia , Colículos Inferiores/parasitologia , Colículos Inferiores/patologia , Leishmania infantum/genética , Leishmaniose Visceral/parasitologia , Leishmaniose Visceral/patologia , Masculino , Reação em Cadeia da Polimerase/veterinária , Telencéfalo/parasitologia , Telencéfalo/patologia , Tálamo/parasitologia , Tálamo/patologiaRESUMO
Zoonotic visceral leishmaniasis is caused by the protozoan Leishmania infantum and little is known about the occurrence and pathogenesis of this parasite in the CNS. The aims of this study were to evaluate the occurrence, viability and load of L. infantum in the CNS, and to identify the neurological histological alterations associated with this protozoan and its co-infections in naturally infected dogs. Forty-eight Leishmania-seropositive dogs from which L. infantum was isolated after necropsy were examined. Cerebrospinal fluid (CSF) samples were analyzed by parasitological culture, quantitative real-time PCR (qPCR) and the rapid immunochromatographic Dual Path Platform test. Brain, spinal cord and spleen samples were submitted to parasitological culture, qPCR, and histological techniques. Additionally, anti-Toxoplasma gondii and anti-Ehrlichia canis antibodies in serum and distemper virus antigens in CSF were investigated. None of the dogs showed neurological signs. All dogs tested positive for L. infantum in the CNS. Viable forms of L. infantum were isolated from CSF, brain and spinal cord in 25% of the dogs. Anti-L. infantum antibodies were detected in CSF in 61% of 36 dogs. Inflammatory histological alterations were observed in the CNS of 31% of the animals; of these, 66% were seropositive for E. canis and/or T. gondii. Amastigote forms were associated with granulomatous non-suppurative encephalomyelitis in a dog without evidence of co-infections. The highest frequency of L. infantum DNA was observed in the brain (98%), followed by the spinal cord (96%), spleen (95%), and CSF (50%). The highest L. infantum load in CNS was found in the spinal cord. These results demonstrate that L. infantum can cross the blood-brain barrier, spread through CSF, and cause active infection in the entire CNS of dogs. Additionally, L. infantum can cause inflammation in the CNS that can lead to neurological signs with progression of the disease.
Assuntos
Doenças do Sistema Nervoso Central/veterinária , Doenças do Cão/parasitologia , Leishmania infantum/fisiologia , Leishmaniose Visceral/veterinária , Animais , Anticorpos Antibacterianos/sangue , Anticorpos Antibacterianos/imunologia , Anticorpos Antiprotozoários/sangue , Anticorpos Antiprotozoários/imunologia , Sistema Nervoso Central/parasitologia , Sistema Nervoso Central/patologia , Doenças do Sistema Nervoso Central/líquido cefalorraquidiano , Doenças do Sistema Nervoso Central/parasitologia , Coinfecção/microbiologia , Coinfecção/parasitologia , Coinfecção/veterinária , DNA de Protozoário/genética , Doenças do Cão/microbiologia , Cães , Ehrlichia canis/imunologia , Ehrlichia canis/fisiologia , Ehrlichiose/microbiologia , Ehrlichiose/veterinária , Interações Hospedeiro-Parasita , Interações Hospedeiro-Patógeno , Hibridização In Situ , Leishmania infantum/genética , Leishmania infantum/imunologia , Leishmaniose Visceral/líquido cefalorraquidiano , Leishmaniose Visceral/parasitologia , Carga Parasitária , Reação em Cadeia da Polimerase em Tempo Real , Toxoplasma/imunologia , Toxoplasma/fisiologia , Toxoplasmose/parasitologiaRESUMO
Infection by the rat lungworm Angiostrongylus cantonensis represents the most common cause of infectious eosinophilic meningitis in humans, causing central nervous system (CNS) angiostrongyliasis. Most of CNS angiostrongyliasis cases were described in Asia, Pacific Basin, Australia, and some limited parts of Africa and America. CNS angiostrongyliasis has been reported in the Caribbean but never in the Lesser Antilles. The primary objectives of this study were to depict the first case of CNS angiostrongyliasis in the Lesser Antilles and investigate the environmental presence of A. cantonensis in Guadeloupe, Lesser Antilles. In December 2013, a suspected case of CNS angiostrongyliasis in an 8-month-old infant in Guadeloupe was investigated by real-time polymerase chain reaction (PCR) testing on cerebral spinal fluid (CSF). The environmental investigation was performed by collecting Achatina fulica molluscs from different parts of Guadeloupe and testing the occurrence of A. cantonensis by real-time PCR. CSF from the suspected case of angiostrongyliasis was positive for A. cantonensis by real-time PCR. Among 34 collected snails for environmental investigation, 32.4% were positive for A. cantonensis. In conclusion, we report the first laboratory-confirmed case of CNS-angiostrongyliasis in the Lesser Antilles. We identified the presence and high prevalence of A. cantonensis in A. fulica in Guadeloupe. These results highlight the need to increase awareness of this disease and implement public health programs in the region to prevent human cases of angiostrongyliasis and improve management of eosinophilic meningitis patients.
Assuntos
Angiostrongylus cantonensis/isolamento & purificação , Infecções por Strongylida/diagnóstico , Corticosteroides/uso terapêutico , Albendazol/uso terapêutico , Angiostrongylus cantonensis/genética , Animais , Ásia , Austrália , Sistema Nervoso Central/parasitologia , Sistema Nervoso Central/patologia , Guadalupe , Humanos , Lactente , Ivermectina/uso terapêutico , Reação em Cadeia da Polimerase em Tempo Real , Caramujos/parasitologia , Infecções por Strongylida/tratamento farmacológicoRESUMO
This study was developed in order to describe the early morphological events observed during the invasion of two pathogenic strains of Acanthamoeba (genotype T4); A. castellanii and A. culbertsoni, at the olfactory meatus and cerebral, pulmonary, renal, hepatic and splenic tissues levels, an in vivo invasion study. Histological and immunohistochemical description of the events at 24, 48, 72, and 96 h postintranasal inoculations of BALB/c mice was performed. A. castellanii showed a higher invasion rate than A. culbertsoni, which was only able to reach lung and brain tissue in the in vivo model. The current study supports previous evidence of lack of inflammatory response during the early stages of infection. Acanthamoeba invasion of the CNS and other organs is a slow and contact-dependent process. The early morphological events during the invasion of amoebae include the penetration of trophozoites into different epithelia: olfactory, respiratory, alveolar space, and renal tubule, which resemble the process of amoebae invasion described in corneal tissue. The data suggest that after reaching the nasal epithelium, trophozoites continued invasion, separating and lifting the most superficial cells, then migrating and penetrating between the cell junctions without causing a cytolytic effect on adjacent cells. These results reaffirm the idea that contact-dependent mechanisms are relevant for amoebae of Acanthamoeba genus regardless of the invasion site.
Assuntos
Acanthamoeba/patogenicidade , Amebíase/patologia , Sistema Nervoso Central/parasitologia , Túbulos Renais/parasitologia , Mucosa Nasal/parasitologia , Mucosa Respiratória/parasitologia , Trofozoítos/metabolismo , Animais , Córnea/parasitologia , Modelos Animais de Doenças , Genótipo , Imuno-Histoquímica , Camundongos , Camundongos Endogâmicos BALB CRESUMO
We describe a case of human lagochilascariasis, with skull-base involvement and a chronic and relapsing course after treatment. This rare parasitic infection is usually manifested in the head and neck area, characterized by progressive granulomatous inflammation and the formation of abscesses. Transmission to humans most likely occurs by the consumption of undercooked meat of wild rodents. On the basis of literature studies, we propose the most likely life cycle of the parasite that involves wild feline and rodent species, with humans as accidental hosts. Even in endemic areas, it is very difficult to recognize the disease at an early stage. Progression will eventually lead to involvement of the (central) nervous system, as described in our case. Treatment is often difficult and involves resection and prolonged treatment with anthelmintic drugs. Recurrences are not uncommon and at present, long-term oral administration of ivermectin seems to be the most effective treatment.
Assuntos
Ascaríase/diagnóstico , Base do Crânio/parasitologia , Abscesso/diagnóstico , Abscesso/parasitologia , Adulto , Animais , Anti-Helmínticos/uso terapêutico , Ascaríase/tratamento farmacológico , Ascaríase/transmissão , Gatos/parasitologia , Sistema Nervoso Central/parasitologia , Contaminação de Alimentos , Parasitologia de Alimentos , Cabeça/parasitologia , Humanos , Ivermectina/uso terapêutico , Masculino , Carne/parasitologia , Pescoço/parasitologia , Roedores/parasitologia , SurinameRESUMO
The existence of the nervous form of Chagas disease is a matter of discussion since Carlos Chagas described neurological disorders, learning and behavioural alterations in Trypanosoma cruzi-infected individuals. In most patients, the clinical manifestations of the acute phase, including neurological abnormalities, resolve spontaneously without apparent consequence in the chronic phase of infection. However, chronic Chagas disease patients have behavioural changes such as psychomotor alterations, attention and memory deficits, and depression. In the present study, we tested whether or not behavioural alterations are reproducible in experimental models. We show that C57BL/6 mice chronically infected with the Colombian strain of T. cruzi (150 days post-infection) exhibit behavioural changes as (i) depression in the tail suspension and forced swim tests, (ii) anxiety analysed by elevated plus maze and open field test sand and (iii) motor coordination in the rotarod test. These alterations are neither associated with neuromuscular disorders assessed by the grip strength test nor with sickness behaviour analysed by temperature variation sand weight loss. Therefore, chronically T. cruzi-infected mice replicate behavioural alterations (depression and anxiety) detected in Chagas disease patients opening an opportunity to study the interconnection and the physiopathology of these two biological processes in an infectious scenario.
Assuntos
Ansiedade/parasitologia , Doença de Chagas/complicações , Depressão/parasitologia , Comportamento de Doença , Atividade Motora , Trypanosoma cruzi , Animais , Escala de Avaliação Comportamental , Sistema Nervoso Central/parasitologia , Doença Crônica , Modelos Animais de Doenças , Feminino , Elevação dos Membros Posteriores , Camundongos Endogâmicos C57BL , Força Muscular/fisiologia , Parasitemia/mortalidade , Esforço Físico , Equilíbrio Postural/fisiologia , Desempenho Psicomotor/fisiologia , NataçãoRESUMO
The existence of the nervous form of Chagas disease is a matter of discussion since Carlos Chagas described neurological disorders, learning and behavioural alterations in Trypanosoma cruzi-infected individuals. In most patients, the clinical manifestations of the acute phase, including neurological abnormalities, resolve spontaneously without apparent consequence in the chronic phase of infection. However, chronic Chagas disease patients have behavioural changes such as psychomotor alterations, attention and memory deficits, and depression. In the present study, we tested whether or not behavioural alterations are reproducible in experimental models. We show that C57BL/6 mice chronically infected with the Colombian strain of T. cruzi (150 days post-infection) exhibit behavioural changes as (i) depression in the tail suspension and forced swim tests, (ii) anxiety analysed by elevated plus maze and open field test sand and (iii) motor coordination in the rotarod test. These alterations are neither associated with neuromuscular disorders assessed by the grip strength test nor with sickness behaviour analysed by temperature variation sand weight loss. Therefore, chronically T. cruzi-infected mice replicate behavioural alterations (depression and anxiety) detected in Chagas disease patients opening an opportunity to study the interconnection and the physiopathology of these two biological processes in an infectious scenario.
Assuntos
Animais , Feminino , Ansiedade/parasitologia , Doença de Chagas/complicações , Depressão/parasitologia , Comportamento de Doença , Atividade Motora , Trypanosoma cruzi , Escala de Avaliação Comportamental , Doença Crônica , Sistema Nervoso Central/parasitologia , Modelos Animais de Doenças , Elevação dos Membros Posteriores , Força Muscular/fisiologia , Esforço Físico , Parasitemia/mortalidade , Equilíbrio Postural/fisiologia , Desempenho Psicomotor/fisiologia , NataçãoRESUMO
BACKGROUND: Neospora caninum is an apicomplexan protozoan that is considered one of the main agents responsible for abortion in ruminants. The lesions found in the central nervous system (CNS) of aborted fetuses show multifocal necrosis, gliosis, and perivascular cuffs of mononuclear cells, but the inflammatory and glial cells have not been immunophenotypically characterized. The lesions in the CNS of infected adult animals have rarely been described. Therefore, in this study, we characterized the lesions, the immunophenotypes of the inflammatory and glial cells and the expression of MHC-II and PCNA in the CNS of goats infected with N. caninum. The CNS of eight aborted fetuses and six adult male goats naturally infected with N. caninum were analyzed with lectin histochemistry (RCA1) and immunohistochemistry (with anti-CD3, -CD79α, -GFAP, -MHC-II, and -PCNA antibodies). All animals were the offspring of dams naturally infected with N. caninum. RESULTS: The microscopic lesions in the CNS of the aborted fetuses consisted of perivascular cuffs composed mainly of macrophages (RCA1(+)), rare T lymphocytes (CD3(+)), and rare B lymphocytes (CD79α(+)). Multifocal necrosis surrounded by astrocytes (GFAP(+)), gliosis composed predominantly of monocytic-lineage cells (macrophages and microglia, RCA1(+)), and the cysts of N. caninum, related (or not) to the lesions were present. Similar lesions were found in four of the six male goats, and multinucleate giant cells related to focal gliosis were also found in three adult goats. Anti-GFAP immunostaining showed astrocytes characterizing areas of glial scarring. Cysts of N. caninum were found in three adult male goats. The presence of N. caninum was evaluated with histopathology, immunohistochemistry, and PCR. Immunohistochemistry demonstrated anti-PCNA labeling of macrophages and microglia in the perivascular cuffs and the expression of MHC-II by microglia and endothelial cells in the CNS of the aborted fetuses and adult male goats. CONCLUSIONS: Macrophages and microglia were the predominant inflammatory cells in the CNS of aborted fetuses and healthy adult male goats infected with N. caninum. Activated astrocytes were mainly associated with inflamed areas, suggesting that astrocytes were involved in the resolution of the lesions.
Assuntos
Sistema Nervoso Central/parasitologia , Coccidiose/veterinária , Doenças das Cabras/patologia , Neospora , Neuroglia/parasitologia , Animais , Sistema Nervoso Central/embriologia , Sistema Nervoso Central/patologia , Coccidiose/patologia , Doenças das Cabras/embriologia , Doenças das Cabras/parasitologia , Cabras/embriologia , Cabras/parasitologia , Masculino , Neuroglia/patologiaRESUMO
Angiostrongylus cantonensis is a zoonotic pathogen that occasionally causes human angiostrongyliasis; its main clinical manifestation is eosinophilic meningitis. This report defines the concept of intrathecal activation of complement as evidence of intrathecal synthesis of major immunoglobulins during this disease. Details are presented of the activation of complement system components in cerebrospinal fluid, and their application to our understanding of this tropical disease, which is emerging in the Western hemisphere. Intrathecal synthesis of at least one of the major immunoglobulins and a wide spectrum of patterns may be observed. Although intrathecal synthesis of C3c is always present, C4 intrathecal synthesis does not occur in every patient. The diversity of intrathecal synthesis and activation of the different complement pathways enables their division into three variant groups (A, B, and C). Variant group A includes the classical and/or lectin pathway and involves two or more major immunoglobulins with C3 and C4 intrathecal synthesis. Variant group B involves C4 in cerebrospinal fluid that comes from blood in the intrathecal activation of the classical pathway. Variant group C includes the alternative pathway.
Assuntos
Sistema Nervoso Central/imunologia , Sistema Nervoso Central/parasitologia , Infecções por Strongylida/imunologia , Angiostrongylus cantonensis/isolamento & purificação , Angiostrongylus cantonensis/patogenicidade , Animais , Complemento C3c/líquido cefalorraquidiano , Complemento C3c/imunologia , Complemento C4b/líquido cefalorraquidiano , Complemento C4b/imunologia , Eosinofilia/líquido cefalorraquidiano , Eosinofilia/imunologia , Eosinofilia/parasitologia , Humanos , Imunoglobulinas/líquido cefalorraquidiano , Imunoglobulinas/imunologia , Meningite/líquido cefalorraquidiano , Meningite/imunologia , Meningite/parasitologia , Fragmentos de Peptídeos/líquido cefalorraquidiano , Fragmentos de Peptídeos/imunologia , Infecções por Strongylida/líquido cefalorraquidiano , Infecções por Strongylida/parasitologiaRESUMO
BACKGROUND: Neurocysticercosis (NCC) is the most common parasitic infection in the central nervous system and the most common cause of acquired neurological symptoms in young adults living in developing countries. Many "asymptomatic" patients begin experiencing neurological symptoms after the use of antiparasitic drugs for gastrointestinal treatment. Patients who are previously diagnosed with NCC require special care during cysticidal treatment because of the inflammatory effects caused by the interaction between the drug, the parasite, and the host. CASE DESCRIPTION: Of a series of 46 cases, we selected five patients with a history of being "asymptomatic" and who began experiencing neurologic symptoms after the use of albendazole, which led to a diagnosis of cysticercosis. Another case of the patient, who already had been diagnosed of ventricular cysticercosis, was given a drug treatment without consulting the neurosurgeon and had a fatal outcome attributable to secondary meningoencephalitis. RESULTS: In the first five cases, with new neurological symptoms after antihelmintic treatment, the self-prescription is remarkable. The symptoms appear between the third and fifth day of treatment. All of them had a clinical course without complications. Only two cases minimally invasive techniques were required. The case who had been already diagnosed developed meningoencephalitis and died after eight days of antihelmintic treatment. CONCLUSIONS: Anthelminthic drug treatment requires tailor-based prescription considering risk-benefit ratio with the drug-parasite-host interaction in mind. Treatment is not harmless so patients have to be closely watched. In select cases, medical treatment cannot replace surgical procedures, which can be the primary approach with drug treatment as a complement.
Assuntos
Albendazol/administração & dosagem , Albendazol/efeitos adversos , Sistema Nervoso Central/efeitos dos fármacos , Neurocisticercose/tratamento farmacológico , Adolescente , Adulto , Anti-Helmínticos/administração & dosagem , Anti-Helmínticos/efeitos adversos , Sistema Nervoso Central/imunologia , Sistema Nervoso Central/parasitologia , Infecções Protozoárias do Sistema Nervoso Central/tratamento farmacológico , Infecções Protozoárias do Sistema Nervoso Central/imunologia , Infecções Protozoárias do Sistema Nervoso Central/cirurgia , Monitoramento de Medicamentos , Evolução Fatal , Feminino , Interações Hospedeiro-Parasita/efeitos dos fármacos , Interações Hospedeiro-Parasita/imunologia , Humanos , Masculino , Neurocisticercose/imunologia , Neurocisticercose/cirurgia , Adulto JovemRESUMO
A neurocisticercose é uma doença caracterizada pelo envolvimento do sistema nervoso central pelo estágio larval intermediário do parasita Taenia solium. O processo de degeneração da larva e a reação inflamatória do organismo causam os sintomas clínicos. Relatamos a reativação clínica e radiológica de uma forma nodular calcificada e assintomática há mais de 20 anos. O tratamento antiparasitário mostrou boa resposta.
Neurocysticercosis is a disease characterized by the involvement of the central nervous system by the intermediate larval stage of the parasite Taenia solium. The larva degeneration process and the inflammatory reaction of the body cause clinical symptoms. The authors report a case of clinical and radiological reactivation of nodular calcified neurocysticercosis in a patient who was asymptomatic for more than 20 years. Antiparasitic treatment showed a good response.
Assuntos
Humanos , Feminino , Pessoa de Meia-Idade , Calcinose , Tecido Nervoso , Neurocisticercose , Recidiva , Sistema Nervoso Central/anormalidades , Sistema Nervoso Central/parasitologia , Taenia solium , Tontura , Espectroscopia de Ressonância Magnética , Cefaleia , ConvulsõesRESUMO
Trypanosoma cruzi causes a pan-infection, Chagas disease, in American mammals through fecal transmission by triatomine insects, resulting in an acute phase parasitemia with intracellularity mainly in the myocells and cells of the central nervous system (CNS).The parasites, due to the immune response, then decrease in number, characteristic of the life-long chronicity of the disease. We infected a mouse model with isolates obtained from reservoirs and vectors from rural and urban endemic areas in Venezuela. Intracellular proliferation and differentiation of the parasite in astrocytes, microglia, neurons, endothelial cells of the piarachnoid, cells of the Purkinje layer, and spinal ganglion cells, as well as extracellularly in the neuropil, were evaluated during the acute phase. Damages were identified as meningoencephalitis, astrocytosis, reactive microglia, acute neuronal degeneration by central chromatolysis, endothelial cell hyperplasia, edema of the neuropil, and satellitosis. This is the first time that satellitosis has been reported from a mammal infected with T. cruzi. Intracellular T. cruzi and inflammatory infiltrates were found in cardiac and skeletal myocytes and liver cells. No parasitism or alterations to the CNS were observed in the chronic mice, although they did show myocarditis and myocitis with extensive infiltrates. Our results are discussed in relation to hypotheses that deny the importance of the presence of tissue parasites versus the direct relationship between these and the damages produced during the chronic phase of Chagas disease. We also review the mechanisms proposed as responsible for the nervous phase of this parasitosis.
Assuntos
Doenças do Sistema Nervoso Central/parasitologia , Doença de Chagas/parasitologia , Modelos Animais de Doenças , Interações Hospedeiro-Parasita , Trypanosoma cruzi/patogenicidade , Animais , Sistema Nervoso Central/parasitologia , Sistema Nervoso Central/patologia , Doenças do Sistema Nervoso Central/patologia , Doença de Chagas/patologia , Camundongos , VenezuelaRESUMO
Visceral leishmaniasis (VL) is a severe chronic disease caused by Leishmania (Leishmania) infantum chagasi. Better knowledge on the effects caused by this disease can help develop adequate clinical management and treatment. Parasitological and immunohistochemical studies were performed golden hamsters Mesocricetus auratus infected with bone marrow from individuals with VL in the State of Mato Grosso do Sul, central-west Brazil. The effects of parasitism in the spleen, liver, kidneys, lungs, heart and brain of the animals were examined. Eighteen hamsters were inoculated intraperitoneally, and six healthy animals were used as negative controls. The animals were kept in the animal house and checked for clinical signs. Specimens of each organ were examined for the presence of amastigotes. Immunohistochemical technique was performed in all brain specimens and organs negative on the direct examination of parasites. Direct examination of amastigotes was positive in the spleen and liver of all infected animals; 33.3% showed the parasite in the kidneys and lungs, and 16.7% in the heart. Parasitic forms were seen in 83.3% (15/18) of the brain examined. Immunohistochemistry confirmed the results of the direct examination, except in two specimens of lung tissue and in the brain specimens. Other studies are needed to further clarify the effect of the parasite in the central nervous system.(AU)
A leishmaniose visceral (LV) é uma doença crônica grave, causada pelo parasito Leishmania (Leishmania) infantum chagasi. Esclarecer as alterações provocadas pela doença é fundamental para que se adotem condutas clínicas e de tratamento adequadas. Com o objetivo de analisar a infecção experimental em hamsters da linhagem golden, Mesocricetus auratus, infectados com tecido de medula óssea de pacientes com LV no Estado de Mato Grosso do Sul, foram realizados estudos parasitológicos e de imunomarcação. Foi verificada a distribuição do parasitismo no baço, fígado, rim, pulmão, coração e encéfalo desses animais. Foram utilizados 18 hamsters experimentalmente inoculados via intra-peritoneal, e seis animais sadios como controles negativos. Os animais foram mantidos em biotério de experimentação e observados, em busca de alterações clínicas. Com fragmentos de cada órgão, procedeu-se a confecção de lâminas por aposição para pesquisa de amastigotas. Nos órgãos com resultado negativo na pesquisa direta do parasito, e em todas as amostras de encéfalo, foi realizada a técnica de imunohistoquímica. A pesquisa direta de amastigotas foi positiva no baço e fígado de todos os animais infectados; 33,3% apresentaram o parasito em rim e pulmão, e 16,7% no coração. Quando realizada a pesquisa em encéfalo, formas parasitárias foram observadas em 83,3% (15/18) dos animais. A imunomarcação confirmou os resultados da pesquisa direta, exceto em duas amostras de tecido pulmonar e nas amostras de encéfalo. Mais estudos são necessários, para esclarecer o real papel do parasito no sistema nervoso central.(AU)
Assuntos
Animais , Leishmania/isolamento & purificação , Leishmaniose Visceral/diagnóstico , Mesocricetus/parasitologia , Sistema Nervoso Central/parasitologia , Encéfalo/parasitologia , Imuno-Histoquímica/métodos , Imuno-Histoquímica/veterinária , Baço/parasitologia , Fígado/parasitologia , Rim/parasitologia , Pulmão/parasitologia , Coração/parasitologiaRESUMO
In order to investigate the differential ALCAM, ICAM-1 and VCAM-1 adhesion molecules mRNA expression and the blood-brain barrier (BBB) permeability in C57BL/6 and BALB/c mice in Toxoplasma gondii infection, animals were infected with ME-49 strain. It was observed higher ALCAM on day 9 and VCAM-1 expression on days 9 and 14 of infection in the central nervous system (CNS) of C57BL/6 compared to BALB/c mice. The expression of ICAM-1 was high and similar in the CNS of both lineages of infected mice. In addition, C57BL/6 presented higher BBB permeability and higher IFN-gamma and iNOS expression in the CNS compared to BALB/c mice. The CNS of C57BL/6 mice presented elevated tissue pathology and parasitism. In conclusion, our data suggest that the higher adhesion molecules expression and higher BBB permeability contributed to the major inflammatory cell infiltration into the CNS of C57BL/6 mice that was not efficient to control the parasite.
Assuntos
Molécula de Adesão de Leucócito Ativado/biossíntese , Barreira Hematoencefálica/metabolismo , Encefalite/parasitologia , Toxoplasma/patogenicidade , Toxoplasmose Cerebral/parasitologia , Molécula 1 de Adesão de Célula Vascular/biossíntese , Molécula de Adesão de Leucócito Ativado/genética , Animais , Barreira Hematoencefálica/parasitologia , Sistema Nervoso Central/imunologia , Sistema Nervoso Central/parasitologia , Sistema Nervoso Central/patologia , Encefalite/imunologia , Encefalite/metabolismo , Feminino , Coração/parasitologia , Imuno-Histoquímica , Interferon gama/biossíntese , Interferon gama/genética , Fígado/parasitologia , Fígado/patologia , Pulmão/imunologia , Pulmão/parasitologia , Pulmão/patologia , Camundongos , Camundongos Endogâmicos BALB C , Camundongos Endogâmicos C57BL , Miocárdio/patologia , Óxido Nítrico Sintase Tipo II/biossíntese , Óxido Nítrico Sintase Tipo II/genética , Permeabilidade , RNA Mensageiro/metabolismo , Baço/parasitologia , Baço/patologia , Toxoplasma/imunologia , Toxoplasmose Cerebral/imunologia , Toxoplasmose Cerebral/metabolismo , Molécula 1 de Adesão de Célula Vascular/genéticaRESUMO
Chemokines comprise a structurally related family of cytokines that regulate leukocyte trafficking. Because infection with Toxoplasma gondii can induce an important inflammatory reaction that, if left uncontrolled, can lead to death, we investigated the role of the chemokine receptor CCR2 in T. gondii infection. We orally infected CCR2(-/-) mice with five ME-49 T. gondii cysts and monitored morbidity, survival, and immune response thereafter. The CCR2(-/-) mice displayed higher susceptibility to infection as all mice died on day 28 after infection. Despite similar Th1 responses, a more evident anti-inflammatory response was induced in the peripheral organs of CCR2(-/-) mice compared with wild-type C57BL/6 mice. Additionally, CCR2(-/-) mice presented greater parasitism and a milder inflammatory reaction in their peripheral organs with lesser CD4(+) and MAC-1(+) and greater CD8(+) cell migration. The parasite load decreased in these organs in CCR2(-/-) mice but remained uncontrolled in the central nervous system. Additionally, we observed down-regulated inducible nitric oxide synthase expression in peripheral organs from CCR2(-/-) mice that was associated with a small nitric oxide production by spleen macrophages. In conclusion, in the absence of CCR2, another mechanism is activated to control tissue parasitism in peripheral organs. Nevertheless, CCR2 is essential for the activation of microbicidal mediators that control T. gondii replication in the central nervous system.
Assuntos
Sistema Nervoso Central/imunologia , Sistema Nervoso Central/parasitologia , Receptores CCR2/metabolismo , Toxoplasmose Animal/imunologia , Toxoplasmose Animal/metabolismo , Animais , Movimento Celular , Sistema Nervoso Central/patologia , Quimiocina CCL2/biossíntese , Citocinas/biossíntese , Ensaio de Imunoadsorção Enzimática , Feminino , Citometria de Fluxo , Imuno-Histoquímica , Inflamação/imunologia , Inflamação/parasitologia , Inflamação/patologia , Intestino Delgado/metabolismo , Intestino Delgado/parasitologia , Macrófagos/metabolismo , Camundongos , Camundongos Endogâmicos C57BL , Camundongos Mutantes , Óxido Nítrico/biossíntese , Óxido Nítrico Sintase Tipo II/biossíntese , Linfócitos T/metabolismo , Toxoplasmose Animal/patologiaRESUMO
Trypanosoma cruzi lineages, microsatellite allelic polymorphism, and mithocondrial gene haplotypes were directly typified from peripheral blood and cerebrospinal fluid specimens of a Bolivian patient with Chagas disease with accompanying AIDS and central nervous system severe involvement. Of note, the patient's blood was infected by a mixture of T. cruzi I and T. cruzi IId/e polyclonal populations while the cerebrospinal fluid showed only a monoclonal T. cruzi I population. Our findings do not corroborate the original assumption of innocuity for T. cruzi I in the southern cone of the Americas and highlight lineage I tropism for central nervous system causing lethal Chagas reactivation.