Clusters of Hantavirus Infection, Southern Argentina

Person-to-person transmission should be suspected when Andes virus case-patients are linked

Trypanosoma cruzi Infection Modulates In Vivo Expression of Major Histocompatibility Complex Class II Molecules on Antigen-Presenting Cells and T-Cell Stimulatory Activity of Dendritic Cells in a Strain-Dependent Manner

A striking feature of Chagas' disease is the diversity of clinical presentations. Such variability may be due to the heterogeneity among Trypanosoma cruzi isolates or to the host immune response. Employing two strains which differ in their virulence, we investigated the effect of in vivo infection on professional antigen-presenting cells (APC). Acute infection with the virulent RA strain downregulated the expression of major histocompatibility complex (MHC) class II on splenic dendritic cells (DC) and inhibited its induction on peritoneal macrophages and splenic B cells. It also impaired the ability of DC to prime allogeneic T cells and to form homotypic clusters, suggesting a low maturation state of these cells. In contrast, the low-virulence K98 strain maintained the expression of MHC class II on DC or stimulated it on peritoneal macrophages and B cells and preserved DC's T-cell priming capacity and homotypic clustering. DC from RA-infected mice elicited a lower activation of T. cruzi-specific T-cell proliferation than those from K98-infected mice. APC from RA-infected mice that reached the chronic phase of infection restored MHC class II levels to those found in K98-infected mice and upregulated costimulatory molecules expression, suggesting that the immunosuppression caused by this strain is only transient. Taken together, the results indicate that in vivo infection with T. cruzi modulates APC functionality and that this is accomplished in a strain-dependent manner

Identification of novel vaccine candidates for Chagas' disease by immunization with sequential fractions of a trypomastigote cDNA expression library

The protozoan Trypanosoma cruzi is the etiological agent of Chagas' disease, a major chronic infection in Latin America. Currently, there are neither effective drugs nor vaccines for the treatment or prevention of the disease. Several T. cruzi surface antigens are being tested as vaccines but none of them proved to be completely protective, probably because they represent only a limited repertoire of all the possible T. cruzi target molecules. Taking into account that the trypomastigote stage of the parasite must express genes that allow the parasite to disseminate into the tissues and invade cells, we reasoned that genes preferentially expressed in trypomastigotes represent potential targets for immunization. Here we screened an epimastigote-subtracted trypomastigote cDNA expression library by genetic immunization, in order to find new vaccine candidates for Chagas' disease. After two rounds of immunization and challenge with trypomastigotes, this approach led to the identification of a pool of 28 gene fragments that improved in vivo protection. Sequence analysis of these putative candidates revealed that 19 out of 28 (67.85%) of the genes were hypothetical proteins or unannotated T. cruzi open reading frames, which certainly would not have been identified by other methods of vaccine discovery

Clusters of Hantavirus Infection, Southern Argentina

Fil: Lazaro, María Ester. Hospital Zonal Bariloche; Rio Negro, Argentina.Fil: Cantoni, Gustavo. Unidad Regional de Epidemiología y Salud Ambienta; Rio Negro, Argentina.Fil: Calanni, Liliana. Hospital Castro Rendón; Neuquén, Argentina.Fil: Resa, Amanda J. Hospital de área El Bolsón; Rio Negro, Argentina.Fil: Herrero, Eduardo. Unidad Regional de Epidemiología y Salud Ambienta; Rio Negro, Argentina.Fil: Iacono, Marisa A. Hospital Castro Rendón; Neuquen, Argentina.Fil: Enria, Delia. ANLIS Dr.C.G.Malbrán. Instituto Nacional de Enfermedades Virales Humanas; Argentina.Fil: Cappa, Stella M. González. Universidad de Buenos Aires; Argentina.Person-to-person transmission of a hantavirus was first confirmed during a 1996 outbreak of hantavirus pul- monary syndrome in southern Argentina, where Andes virus is endemic. To identify other episodes of secondary transmission, we reviewed reports of 51 cases of han- tavirus infection from this region (November 1993–June 2005). Nine clusters involving 20 cases (39.2%) were found. Two patients, who had symptoms 3 weeks after they shared risks for rodent exposure, were considered a clus- ter. The other 8 clusters each began with an index case, which was almost always fatal, followed 19–40 days later by the illness of at least 1 person who had close and pro- longed contact with the index case-patient. Person-to-per- son transmission was considered the probable source of these 8 clusters. The probability of initiating secondary cases was 41% for patients who died versus 4% for those who survived (p = 0.005). Interpersonal transmission of Andes virus infection should be considered even when rodent exposure cannot be definitively excluded

Clusters of Hantavirus Infection, Southern Argentina

Fil: Lazaro, María Ester. Hospital Zonal Bariloche; Rio Negro, Argentina.Fil: Cantoni, Gustavo. Unidad Regional de Epidemiología y Salud Ambienta; Rio Negro, Argentina.Fil: Calanni, Liliana. Hospital Castro Rendón; Neuquén, Argentina.Fil: Resa, Amanda J. Hospital de área El Bolsón; Rio Negro, Argentina.Fil: Herrero, Eduardo. Unidad Regional de Epidemiología y Salud Ambienta; Rio Negro, Argentina.Fil: Iacono, Marisa A. Hospital Castro Rendón; Neuquen, Argentina.Fil: Enria, Delia. ANLIS Dr.C.G.Malbrán. Instituto Nacional de Enfermedades Virales Humanas; Argentina.Fil: Cappa, Stella M. González. Universidad de Buenos Aires; Argentina.Person-to-person transmission of a hantavirus was first confirmed during a 1996 outbreak of hantavirus pul- monary syndrome in southern Argentina, where Andes virus is endemic. To identify other episodes of secondary transmission, we reviewed reports of 51 cases of han- tavirus infection from this region (November 1993–June 2005). Nine clusters involving 20 cases (39.2%) were found. Two patients, who had symptoms 3 weeks after they shared risks for rodent exposure, were considered a clus- ter. The other 8 clusters each began with an index case, which was almost always fatal, followed 19–40 days later by the illness of at least 1 person who had close and pro- longed contact with the index case-patient. Person-to-per- son transmission was considered the probable source of these 8 clusters. The probability of initiating secondary cases was 41% for patients who died versus 4% for those who survived (p = 0.005). Interpersonal transmission of Andes virus infection should be considered even when rodent exposure cannot be definitively excluded

High Rate of Strongyloidosis Infection, Out of Endemic Area, in Patients with Eosinophilia and without Risk of Exogenous Reinfections

Strongyloides stercoralis chronic infections are usually asymptomatic and underestimated. We used direct fresh stool examination, Ritchie's method, and agar plate culture for diagnosis in patients with eosinophilia and previous residence in endemic areas. The frequency of strongyloidosis detected among these patients was high: 21 of 42 were positive. Among them, 10 were positive only by agar plate culture. After ivermectin treatment, patients resulted negative for parasitological tests and reduced their eosinophil counts. Half of the submitted patients that were followed 4–12 months after treatment remained negative without eosinophilia, except one who showed an eosinophil ascending curve before reappearance of larvae in stools. The high frequency of strongyloidosis found in this group emphasizes the relevance of including this parasitosis among differential diagnosis in patients with eosinophilia and past risk of S. stercoralis infection to prevent disseminated infections secondary to corticoid therapy