Home Economics American Trypanosomiasis Chagas Disease, Second Edition: One Hundred Years of Research
AIDS and Chagas' disease
Reactivation of chronic stage of Chagas’ disease is uncommon; acute exacerbations of a latent or chronic infection due to T. cruzi can occur in individuals with involvement of cellular immunity, especially in those with advanced HIV/AIDS disease, prolonged corticosteroid use, or other immunosuppressive therapies and transplant- associated immunosuppresion.30,31
In a prospective study that included patients in the pre and post highly active antiretroviral therapy (HAART) era the frequency of reactivation of T. cruzi infection was approximately 20%.32
In patients coinfected with HIV, the reactivation of Chagas’ disease may be related to the selected cellular immune depletion or to the characteristics of the parasite. This situation has been demonstrated by the presence of Trypomastigotes in blood by microhematocrit of quantitative buffy-coat (QBC) and by the invasion of the CNS or the heart.33-35
The majority of the patients present with CNS or myocardial involvement; less frequent clinical manifestations include the digestive tract, especially the esophagus and the colon. Skin lesions, peritoneum involvement, and cervix uteri compromise36 are described infrequently.
Generally, the majority of AIDS patients with reactivated of Chagas’ disease have CD4 T cell counts below 200 cell/pL and, especially, less than 50 cells/pL.
In contrast with heart transplant recipients with reactivated of chronic Chagas’ disease in whom myocarditis is the predominant clinical form of presentation, in AIDS patients, CNS manifestations occur frequently and can include meningoencephalitis or brain masses (named as chagomas). The CNS involvement represents 80-90% of total episodes of reactivation of chronic Chagas’ disease in AIDS patients.37 In patients with cerebral masses, neurological symptoms and signs include headaches, fever, cognitive changes, seizures, or neurological focal signs depending on the number, size, and location of these lesions. On the other hand, patients who develop diffuse meningoencephalitis present with fever, headaches, meningism, and altered mental status.
The CNS tumor-like lesions are, in our experience, the most common clinical manifestation and these are indistinguishable from other opportunistic infections, such as toxoplasmosis or neoplastic process, as primary central nervous system lymphoma (PCNSL) that can involve the CNS in AIDS patients.24
Cerebral chagomas are contrast-enhancing single or multiple focal brain lesions with hypodense areas of perilesional edema and mass effect on the middle line structures (Fig. 30.2). Generally, lesions due to T. cruzi are located in the white matter and occasionally involve the cerebral cortex. In a study by Cordova et al.38 which included 15 patients with reactivation of Chagas’ disease with CNS involvement, the most frequent findings were a single supratentorial hypodense lesion compatible with abscess and involving predominately the white matter of brain lobes (Fig. 30.3). On the contrary, the lesions caused by Toxoplasma gondii frequently compromise the brain cortex, thalamus, and the basal ganglia. In both cases, histopathological examination reveals necrotic encephalitis; however, the multifocal identification of parasites is more frequent in the reactivation of Chagas’ disease than in Toxoplasma encephalitis.
The second most frequent expression of the reactivation of T. cruzi infection in the CNS is the diffuse meningoencephalitis. In these patients the diagnosis is
Figure 30.2 Axial Tl-weighted MRI image shows two large lesions in the right parietal and frontal lobes (arrows), with contrast enhancement, perilesional edema, and mass effect on the middle line structures.
Figure 30.3 CT of the brain showing a single hypodense lesion in the right temporoparietal lobe, with minimum contrast enhancement, no displacement of normal structures, and edema (arrow).
easily confirmed by the lumbar puncture and the centrifugation of cerebrospinal fluid (CSF) with the detection of Trypomastigotes with a Giemsa smear. Lumbar puncture has a high sensitivity for the diagnosis of chagasic meningoencephalitis and should always be performed in the absence of contraindication for it. Cordova et al.38 showed that the sensitivity of this technique was 85%. CSF examination showed typical parasitic meningitis with leptomeningeal involvement and lymphomononuclear pleocytosis.39
Pagano et al.40 studied 10 patients with AIDS and Chagas’ disease. All patients presented cerebral tumor-like lesions and six of them developed intracranial hypertension syndrome. In addition, Cordova et al.38 in 15 patients showed only 2 patients with meningoencephalitis as a unique clinical expression of the disease.
In Argentina, the myocardium is, after the CNS, the second target organ in patients with reactivation of chronic Chagas’ disease and AIDS. Acute myocarditis with arrhythmias and refractory congestive heart failure, with rapid and generally fatal evolution, represents the most frequent clinical presentation. , , Diagnosis of this complication should be suspected in HIV patients with dilated cardiomyopathy, epidemiological antecedents, and positive serologic tests for T. cruzi antibodies. Symptoms and signs are identical to other dilated cardiomyopathies.6,43
Less frequent, medical literature describes the existence of patients with chronic diarrhea and amastigotes of T. cruzi in duodenal biopsy smears prolonged fever and parasitemia.
A high rate of the disease reactivation in the coinfected population may be observed with the central nervous system as the main site of reactivation, representing more than 70% of cases. Some of the predictors of the occurrence of Chagas’ disease reactivation are the detection of parasitemia, low CD4 T lymphocyte values (<200 cells/mm3), and high viral load of HIV, although these are not essential to its occurrence.44
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