Acute   infection is associated with anemia, thrombocytopenia, leukopenia, and bone marrow hypoplasia: reversal by nifurtimox treatment

Marcondes, Maria Cecília Garibaldi; Borelli, Primavera; Yoshida, Nobuko; Russo, Marco

doi:10.1016/s1286-4579(00)00333-6

Cited by 69 publications

(73 citation statements)

References 23 publications

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“…1A). In accordance with a previous study [22], we found a significant reduction in the number of total BM cells 15 days after infection. Further, flow cytometry (FCM) analysis of BM cells revealed that the main population affected by T. cruzi infection displayed a lymphoid morphology (Fig.…”

Section: T Cruzi Infection Induces a Marked Depletion Of Bm Immaturesupporting

confidence: 93%

Depletion of immature B cells duringTrypanosoma cruzi infection: involvement of myeloid cells and the cyclooxygenase pathway

et al. 2005

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The ability of a microorganism to elicit or evade B cell responses represents a determinant factor for the final outcome of an infection. Although pathogens may subvert humoral responses at different stages of B cell development, most studies addressing the impact of an infection on the B cell compartment have focused on mature B cells within peripheral lymphoid organs. Herein, we report that a protozoan infection, i.e. a Trypanosoma cruzi infection, induces a marked loss of immature B cells in the BM, which also compromises recently emigrated B cells in the periphery. The depletion of BM immature B cells is associated with an increased rate of apoptosis mediated by a parasite-indirect mechanism in a Fas/FasL-independent fashion. Finally, we demonstrated that myeloid cells play an important role in B cell depletion, since CD11b + BM cells from infected mice secrete a product of the cyclooxygenase pathway that eliminates immature B cells. These results highlight a previously unrecognized maneuver used by a protozoan parasite to disable B cell generation, limiting host defense and favoring its chronic establishment.

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Section: T Cruzi Infection Induces a Marked Depletion Of Bm Immaturesupporting

confidence: 93%

Depletion of immature B cells duringTrypanosoma cruzi infection: involvement of myeloid cells and the cyclooxygenase pathway

et al. 2005

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“…The lack of positive correlation observed previously may be explained by the heterogeneous genetic background. Data in the literature have shown that in the murine model, alterations in blood cell counts observed in the acute phase of T. cruzi infection are associated with bone marrow suppression of erythrocytes, megakaryocytes, granulocytes and macrophages; their precursors present impaired ability to fully mature (MARCONDES et al, 2000). Anemia was observed among the patients during the acute phase of T. cruzi infection, as also reported previously (DE TITTO; ARAUJO, 1988).…”

Section: Discussionsupporting

confidence: 82%

“…A study on mice reported that T. cruzi sheds trans-sialidase as a virulence factor that induces accelerated platelet depletion, thereby leading to hematological changes (TRIBULATTI et al, 2005). In fact, mice inoculated with different T. cruzi strains show intense thrombocytopenia, neutropenia, eosinophilia, anemia and leukocytosis during the acute phase of infection (MARCONDES et al, 2000). However, despite knowledge of the symptoms, no study has demonstrated the kinetics of hematological alterations occurring during acute and chronic Chagas disease.…”

Section: Introductionmentioning

confidence: 99%

Hematological alterations during experimental canine infection by Trypanosoma cruzi

Guedes

Veloso

Mineo

et al. 2012

Rev. Bras. Parasitol. Vet.

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To confirm that Beagle dogs are a good experimental model for Chagas disease, we evaluated hematological alterations during the acute and chronic phases in Beagle dogs infected with the Y, Berenice-78 (Be-78) and ABC strains of Trypanosoma cruzi, correlating clinical signs with the parasitemia curve. We demonstrate that the acute phase of infection was marked by lethargy and loss of appetite. Simultaneously, we observed anemia, leukocytosis and lymphocytosis. Also,we describe hematological alterations and clinical signs that were positively correlated with the parasitemia during the experimental infection with the three strains of T. cruzi, and demonstrate that experimental infection of Beagle is a trustworthy model for Chagas disease.Keywords: Trypanosoma cruzi, Beagle dogs, parasitemia, lymphocytosis, anemia, leukocytosis. ResumoPara confirmar que cães Beagle são um bom modelo para doença de Chagas, foram avaliadas as alterações hematológicas durante as fases aguda e crônica em cães Beagle infectados com as cepas Y, Berenice-78 (Be-78) e ABC de Trypanosoma cruzi, correlacionando os sinais clínicos com a curva de parasitemia. Foi demonstrado que a fase aguda da infecção foi marcada por letargia e perda de apetite. Simultaneamente, observou-se anemia, leucocitose e linfocitose. Ainda, foram descritas alterações hematológicas e sinais clínicos positivamente correlacionados com a parasitemia durante a infecção experimental com as três cepas de T. cruzi estudadas, demonstrando que a infecção em cães Beagle constitui um modelo fidedigno para a doença de Chagas.

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“…A anemia, já bem descrita em área endêmica, correspondeu a 88% daqueles que apresentaram alterações hematológicas. Em infecção aguda experimental por Trypanosoma cruzi demonstrou-se, pela primeira vez, que as alterações medulares são freqüentes e incluem anemia, trombocitopenia, leucopenia e hipoplasia medular, e que todas essas alterações são reversíveis após tratamento 26 . Assim, esses achados foram por nós corroborados, pois a hipótese de a leucopenia estar sendo induzida pelo benzonidazol é improvável, já que todos os hemogramas foram realizados pouco antes do início da terapêutica específica.…”

Section: Discussionunclassified

Fase aguda da doença de Chagas na Amazônia brasileira: estudo de 233 casos do Pará, Amapá e Maranhão observados entre 1988 e 2005

Pinto

Valente

et al. 2008

Rev. Soc. Bras. Med. Trop.

164

105

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Foram estudados 233 casos de fase aguda da doença de Chagas, oriundos do Pará, Amapá e Maranhão, observados no período de 1988 a 2005, cento e sessenta deles retrospectivamente de 1988 a 2002 e setenta e três prospectivamente de 2003 a 2005. Entre os casos estudados 78,5% (183/233) faziam parte de surtos provavelmente por transmissão oral, acometendo em média 4 pessoas e 21,5% (50/233) eram casos isolados. Foram considerados casos agudos aqueles que apresentaram exames parasitológicos diretos (a fresco, gota espessa ou Quantitative Buffy Coat - QBC) e/ou IgM anti-Trypanosoma cruzi positivos. Foram feitos ainda xenodiagnósticos em 224 pacientes e hemoculturas em 213. Todos foram avaliados clinica e epidemiologicamente. As manifestações clínicas mais freqüentes foram febre (100%), cefaléia (92,3%), mialgia (84,1%), palidez (67%), dispnéia (58,4%), edema de membros inferiores (57,9%), edema de face (57,5%) dor abdominal (44,2%), miocardite (39,9%) e exantema (27%). O eletrocardiograma mostrou alterações de repolarização ventricular em 38,5% dos casos, baixa voltagem de QRS em 15,4% e desvio de SAQRS em 11,5%, extra-sístoles ventriculares em 5,8%, bradicardia em 5,8% e taquicardia em 5,8%, bloqueio de ramo direito em 4,8% e fibrilação atrial em 4,8%. A alteração mais freqüente vista no ecocardiograma foi o derrame pericárdico em 46,2% dos casos. Treze (5,6%) pacientes evoluíram para o óbito, 10 (76,9%) dos quais por comprometimento cardiovascular, dois por complicações de origem digestiva e um de causa mal definida.

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Acute infection is associated with anemia, thrombocytopenia, leukopenia, and bone marrow hypoplasia: reversal by nifurtimox treatment

Cited by 69 publications

References 23 publications

Depletion of immature B cells duringTrypanosoma cruzi infection: involvement of myeloid cells and the cyclooxygenase pathway

Depletion of immature B cells duringTrypanosoma cruzi infection: involvement of myeloid cells and the cyclooxygenase pathway

Hematological alterations during experimental canine infection by Trypanosoma cruzi

Fase aguda da doença de Chagas na Amazônia brasileira: estudo de 233 casos do Pará, Amapá e Maranhão observados entre 1988 e 2005

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