Trypanosoma cruzi loop-mediated isothermal amplification (Trypanosoma cruzi Loopamp) kit for detection of congenital, acute and Chagas disease reactivation.

A Trypanosoma cruzi Loopamp kit was recently developed as a ready-to-use diagnostic method requiring minimal laboratory facilities. We evaluated its diagnostic accuracy for detection of acute Chagas disease (CD) in different epidemiological and clinical scenarios. In this retrospective study, a convenience series of clinical samples (venous blood treated with EDTA or different stabilizer agents, heel-prick blood in filter paper or cerebrospinal fluid samples (CSF)) from 30 infants born to seropositive mothers (13 with congenital CD and 17 noninfected), four recipients of organs from CD donors, six orally-infected cases after consumption of contaminated guava juice and six CD patients coinfected with HIV at risk of CD reactivation (N = 46 patients, 46 blood samples and 1 CSF sample) were tested by T. cruzi Loopamp kit (Tc LAMP) and standardized quantitative real-time PCR (qPCR). T. cruzi Loopamp accuracy was estimated using the case definition in the different groups as a reference. Cohen's kappa coefficient (κ) was applied to measure the agreement between Tc LAMP (index test) and qPCR (reference test). Sensitivity and specificity of T. cruzi Loopamp kit in blood samples from the pooled clinical groups was 93% (95% CI: 77-99) and 100% (95% CI: 80-100) respectively. The agreement between Tc LAMP and qPCR was almost perfect (κ = 0.92, 95% CI: 0.62-1.00). The T. cruzi Loopamp kit was sensitive and specific for detection of T. cruzi infection. It was carried out from DNA extracted from peripheral blood samples (via frozen EDTA blood, guanidine hydrochloride-EDTA blood, DNAgard blood and dried blood spots), as well as in CSF specimens infected with TcI or TcII/V/VI parasite populations. The T. cruzi Loopamp kit appears potentially useful for rapid detection of T. cruzi infection in congenital, acute and CD reactivation due to HIV infection.

Reactivación de la enfermedad de Chagas en el sistema nervioso central de pacientes infectados por el virus de la inmunodeficiencia humana / Central nervous system reactivation of Chagas' disease in HIV-infected patients

La reactivación de la enfermedad de Chagas (ECH) en pacientes infectados por el virus de la inmunodeficiencia humana (VIH) puede causar lesiones cerebrales ocupantes. Considerando que el diseño de un algoritmo para el diagnóstico precoz podría reducir la mortalidad, deben considerarse diversos escenarios: 1) ¿Cuándo debe indicarse el examen parasitológico (EP) del frotis de sangre periférica y líquido cefalorraquídeo (LCR)? 2) ¿debe realizarse aún en aquellos pacientes con serología negativa para Trypanosoma cruzi?, 3) ¿en qué casos el tratamiento para la encefalitis por T. gondii puede interrumpirse?

Reactivation of Chagas disease (CHD) in patients infected with Human Immunodeficiency Virus (HIV) can cause brain mass lesions. As the design of an algorithm for early diagnosis could reduce mortality, different secenarios should be considered:1) when the parasitologic examination (PE) of peripheral blood smears and cerebrospinal fluid(CSF) should be indicated? 2) should it de performed even in patients with negative serology for Trypanosoma cruzi? 3) in which cases the treatment for T. gondii encephalitis can be discontinued?

Reactivación de la enfermedad de Chagas en el sistema nervioso central de pacientes infectados por el virus de la inmunodeficiencia humana / Central nervous system reactivation of Chagas disease in HIV-infected patients

La reactivación de la enfermedad de Chagas (ECH) en pacientes infectados por el virus de la inmunodeficiencia humana (VIH) puede causar lesiones cerebrales ocupantes. Considerando que el diseño de un algoritmo para el diagnóstico precoz podría reducir la mortalidad, deben considerarse diversos escenarios: 1) ¿Cuándo debe indicarse el examen parasitológico (EP) del frotis de sangre periférica y líquido cefalorraquídeo (LCR)? 2) ¿debe realizarse aún en aquellos pacientes con serología negativa para Trypanosoma cruzi?, 3) ¿en qué casos el tratamiento para la encefalitis por T. gondii puede interrumpirse?(AU)

Reactivation of Chagas disease (CHD) in patients infected with Human Immunodeficiency Virus (HIV) can cause brain mass lesions. As the design of an algorithm for early diagnosis could reduce mortality, different secenarios should be considered:1) when the parasitologic examination (PE) of peripheral blood smears and cerebrospinal fluid(CSF) should be indicated? 2) should it de performed even in patients with negative serology for Trypanosoma cruzi? 3) in which cases the treatment for T. gondii encephalitis can be discontinued?(AU)

Tumor-like lesion due to Chagas' disease in a patient with lymphocytic leukemia.

A 73 year-old white male, living in the interior of the state of Mato Grosso do Sul, in central Brazil, after an initial diagnosis of sinusitis was transferred to the neurology service with a 3-day evolution of intracranial hypertension. Exams showed lymphocytic leukemia and a tumor-like lesion, either an expanding inflammatory process such as an abscess or a neoplasm. Treatment with Ceftriaxone and Decadron was started and intracranial hypertension was controlled. Methotrexate was injected on the occasion of the next puncture considering a possible leukemia infiltration. Flagellate forms of T. cruzi were observed in the CSF and treatment with Benznidazole was started. After 4 days the CSF presented fractionated forms of trypomastigotes. The protein level was 27%. Signs of intracranial hypertension ceased. Tomography and magnetic resonance images showed an important reduction of the tumor-like lesion. The clinical condition of the patient improved.

Trypanosoma cruzi meningoencephalitis in AIDS mimicking cerebral metastases: case report

A case of Chagas' meningoencephalitis in a 47 year-old patient with AIDS is presented. The diagnosis was established by examination of the cerebrospinal fluid which showed the presence of Trypanosoma cruzi. CT-scan revealed multiple cerebral lesions which only became evident by contrast administration. A second CT after 13 days showed a severe evolution with displacement of the midline structures leading to the patient's death. This case, as well as other case reports published, has shown the fulminant evolution of Chagas'meningoencephalitis in AIDS patients and the importance of cerebrospinal fluid examination for the diagnosis.

Chagasic meningoencephalitis with detection of Trypanosoma cruzi in the cerebrospinal fluid of an immunodepressed patient.

We report a case of chagasic meningoencephalitis with the detection of Trypanosoma cruzi in the cerebrospinal fluid (CSF). The patient was a renal transplant recipient with a chagasic history preceding surgery who had been receiving immunosuppressive medication for 8 years, a probable cause of the recrudescence of Chagas' disease. He was treated with benznidazole, with normalization of the CSF. He was discharged from hospital in a good clinical condition.

Acute CNS infection by Trypanosoma cruzi (Chagas' disease) in immunosuppressed patients.

Acute CNS involvement by Trypanosoma cruzi is uncommon. We report 2 immunosuppressed patients, 1 adult who developed an acute meningoencephalitis, and 1 child who presented with the tumor-like form of the disease. Both patients acquired the disease through blood transfusion. Blood donors migrating from endemic areas can transmit the disease in nonendemic countries if they are not routinely screened for antibodies to T cruzi.

[Trypanosoma cruzi antibodies in the cerebrospinal fluid: a search using complement fixation and immunofluorescence reactions]. / Anticorpos a trypanosoma cruzi no líquido cefalorraqueano: pesquisa pelas reações de fixação do complemento e de imunofluorescência.

Cerebrospinal fluid (CSF) samples of 200 patients who presented central nervous system (CNS) pathologies were evaluated for antibodies to Trypanosoma cruzi (T. cruzi). The evaluation was made through: complement fixation test (CFT) in 69 patients, indirect (IgG) immunofluorescence test (IFT) in 118, and by CFT and IFT in 13. In 50 cases the IFT has been made also in concentrated (20 X) CSF samples. Results were evaluated in report to CNS pathology, CSF cells and proteins, and tests in the CSF for other CNS infections (syphilis, cysticercosis, schistosomiasis, toxoplasmosis). These tests were based on techniques similar to those adopted for the search of antibodies to T. cruzi, and were conducted concomitantly to tests for T. cruzi in the same CSF sample for everyone of the cases. Antibodies to T. cruzi were found in three patients. The first was a patient committed by the acquired immunodeficiency syndrome (AIDS) in whom there occurred exacerbation of the acute stage of Chagas' disease. The second is a patient who is committed by epilepsy, and an acute stroke occurred in the third patient: Chagas' disease had been previously diagnosed in them through the demonstration of antibodies to T. cruzi in the blood serum.

Blood and cerebrospinal fluid anomalies in brain ageing and Alzheimer's disease.

The glial fibrillary acidic protein (GFAP), myelin basic protein (MBP), S100 protein (S100), gamma gamma-enolase and neurofilament proteins were determined in the CSF of neurological patients. In Alzheimer's disease (AD), the GFAP values were very often increased but this was not specific to this disease. In 2 cases of familial AD, increases in neurofilament protein were detected. The determination of autoantibodies against neurofilament proteins in blood showed rather low values in AD, although they were higher than in subacute sclerosing panencephalitis (SSPE) and Chagas' disease. Increases were observed in diseases not related to AD such as vascular disorders and Parkinson's disease.