Neurological manifestations of Chagas' disease

Córdova, Ezequiel; Maiolo, Elena; Corti, Marcelo; Orduña, Tomás

doi:10.1179/016164110x12644252260637

Cited by 68 publications

(69 citation statements)

References 36 publications

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“…Even among patients without clinical reactivation, the level of parasitemia is higher among HIV-coinfected than among HIV-negative patients (261). Symptomatic T. cruzi reactivation in AIDS patients is most commonly reported to cause meningoencephalitis and/or T. cruzi brain abscesses; the presentation may be confused with CNS toxoplasmosis and should be considered in the differential diagnosis of mass lesions on imaging or CNS syndromes in AIDS patients (70,71,88,260). The second most commonly reported sign of reactivation is acute myocarditis, sometimes superimposed on preexisting chronic Chagas' cardiomyopathy (260,297).…”

Section: T Cruzi Infection In the Immunocompromised Hostmentioning

confidence: 99%

Trypanosoma cruzi and Chagas' Disease in the United States

et al. 2011

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SUMMARY Chagas' disease is caused by the protozoan parasite Trypanosoma cruzi and causes potentially life-threatening disease of the heart and gastrointestinal tract. The southern half of the United States contains enzootic cycles of T. cruzi , involving 11 recognized triatomine vector species. The greatest vector diversity and density occur in the western United States, where woodrats are the most common reservoir; other rodents, raccoons, skunks, and coyotes are also infected with T. cruzi. In the eastern United States, the prevalence of T. cruzi is highest in raccoons, opossums, armadillos, and skunks. A total of 7 autochthonous vector-borne human infections have been reported in Texas, California, Tennessee, and Louisiana; many others are thought to go unrecognized. Nevertheless, most T. cruzi -infected individuals in the United States are immigrants from areas of endemicity in Latin America. Seven transfusion-associated and 6 organ donor-derived T. cruzi infections have been documented in the United States and Canada. As improved control of vector- and blood-borne T. cruzi transmission decreases the burden in countries where the disease is historically endemic and imported Chagas' disease is increasingly recognized outside Latin America, the United States can play an important role in addressing the altered epidemiology of Chagas' disease in the 21st century.

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Section: T Cruzi Infection In the Immunocompromised Hostmentioning

confidence: 99%

Trypanosoma cruzi and Chagas' Disease in the United States

et al. 2011

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“…Damage to the parasympathetic nervous system may be one of the primary events in the pathogenesis of symptomatic Chagas disease and may contribute to heart and gastrointestinal Chagas disease in this way [44,45] . It is assumed that the damage to the parasympathetic nervous system starts in the acute phase and proceeds into the chronic phase.…”

Section: The Nervous System In Chronic Chagas Diseasementioning

confidence: 99%

Chronic Chagas disease: from basics to laboratory medicine

Haberland

Saravia

Wallukat

et al. 2012

Clinical Chemistry and Laboratory Medicine (CCLM)

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Chagas disease, caused by Trypanosoma cruzi infection, is ranked as the most serious parasitic disease in Latin America and has huge potential to become a worldwide problem, due to increasing migration, and international tourism, as well as infectant transfer by blood contact and transfusion, intrauterine transfer, and organ transplantation. Nearly 30% of chronically-infected patients become symptomatic, often with a latency of 10–30 years, developing life-threatening complications. Of those, nearly 90% develop Chagas heart disease, while the others manifest gastrointestinal disease and neuronal disorders. Besides interrupting the infection cycle and chemotherapeutic infectant elimination, starting therapy early in symptomatic patients is important for counteracting the disease. This would be essentially supported by optimized patient management, involving risk assessment, early diagnosis and monitoring of the disease and its treatment. From economic and logistic viewpoints, the tools of laboratory medicine should be especially able to guarantee this. After summarizing the basics of chronic Chagas disease, such as the epidemiological data, the pathogenetic mechanisms thought to drive symptomatic Chagas disease and also treatment options, we present tools of laboratory medicine that address patient diagnosis, risk assessment for becoming symptomatic and guidance, focusing on autoantibody estimation for risk assessment and heart marker measurement for patient guidance. In addition, increases in levels of inflammation and oxidative stress markers in chronic Chagas disease are discussed.

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“…Meningoencephalitis occurs rarely in acute disease-usually in children less than 2 years of age-and CNS manifestations are not a regular feature in chronic disease (36). However, patients with chronic longstanding asymptomatic infection may recrudesce and develop meningoencephalitis that is clinically and radiologically indistinguishable from toxoplasmosis as a consequence of immunosuppression or AIDS.…”

Section: Chagas' Diseasementioning

confidence: 99%

“…However, patients with chronic longstanding asymptomatic infection may recrudesce and develop meningoencephalitis that is clinically and radiologically indistinguishable from toxoplasmosis as a consequence of immunosuppression or AIDS. Seizures are a common manifestation in this situation (36). T. cruzi can also be transmitted by infected blood or organs, causing acute meningoencephalitis in recipients.…”

Section: Chagas' Diseasementioning

confidence: 99%