Abstract.A study was conducted in Lima, Peru to determine if patients with Strongyloides hyperinfection had human T cell lymphotropic virus type-1 (HTLV-I) infection. The study included patients with Strongyloides hyperinfection and a control group consisted of sex-and age-matched asymptomatic healthy individuals whose stools were negative for Strongyloides. A third group included patients with intestinal strongyloidiasis. Sera from each study subject were tested for HTLV-1/2I by an ELISA and Western blot. The HLTV-1 infection rates (85.7%, 18 of 21) were significantly (P Ͻ 0.001) associated with Strongyloides hyperinfection compared with the control group (4.7%, 1 of 21). The HTLV-1 rate (10%, 6 of 62) for patients with intestinal strongyloidiasis was significantly (P Ͻ 0.001) lower than patients with Strongyloides hyperinfection, but did not differ significantly (P Ͼ 0.05) from the control group. The association of HTLV-1 infection was observed among 17 of 19 patients more than 20 years of age and one of two younger patients. None had HTLV-2 infection. In conclusion, Strongyloides hyperinfection among Peruvian patients was highly associated with HTLV-1 infection.Strongyloides stercoralis is a soil-transmitted intestinal nematode that has been estimated to infect at least 60 million people, especially in tropical and subtropical regions.1 The parasite is unique among the parasitic nematodes because of its ability to multiply within the human host for many decades, with the potential to cause life-threatening disease in immunocompromised patients. The usual route of transmission is by penetration of the skin by filariform larvae (infectious form), following contact with contaminated soil. After migration through the lung, the larvae crawl over the glottis, and are then swallowed and develop to adults in the small bowel mucosa. The uncomplicated intestinal form of disease produces nonspecific abdominal symptoms with or without mild sporadic diarrhea. Many infected patients are completely asymptomatic. 2 However, an autoinfective cycle may develop in a proportion of untreated cases. In these cases, infectious filariform larvae develop in the intestines from rhabditiform larvae. Penetration of the colon or the anal skin by filariform larvae, and migration through lung allow reinfection of the same host. The autoinfective cycle, which usually results in a low-grade, chronic infection in immunocompetent hosts, is poorly understood 3 . A large number of cases of chronic, asymptomatic Strongyloides infections were reported among World War II in Southeast Asian prisoners of war and in refugees up to 40 years after leaving endemic regions. [4][5][6] In contrast to autoinfection, Strongyloides may produce a disseminated infection in immunocompromised hosts incapable of mounting an immune response against the parasite. Massive dissemination of invasive filariform larvae from the colon to the lung, liver, central nervous system, or kidney frequently results in a fatal outcome. Carriage by Strongyloides larvae of enterobacte...
We recommend that all patients with uncomplicated intestinal strongyloidiasis, who fail standard therapy, be studied for HTLV-I infection.
RESUMEN:Objetivo: Estudiar la complicación oportunista producida por la toxoplasmosis en pacientes con Bartonellosis en la fase aguda hemática. Material y Métodos: Estudio prospectivo realizado en 68 pacientes de la fase febril anemizante de la Bartonellosis humana atendidos en el Hospital Nacional Cayetano Heredia. Como criterios de la complicación infecciosa por toxoplasmosis se uso el cuadro clínico ( fiebre de origen desconocido, linfoadenomegalia, etc.) presencia de títulos Ig M positivos (Elisa, IFI) y títulos de Ig G altos (>1/1024 o un incremento más de 4 veces del valor basal) y la presencia en biopsias de taquizoitos de Toxoplasma gondii. Resultados: De 68 pacientes con Bartonellosis en 25 (36.7%) presentaron algunas complicaciones infecciosas, de ellos 5/25 (20%) fueron debidas a toxoplasmosis reactivada. El cuadro clínico sistémico de la toxoplasmosis se caracterizó por presencia de fiebre en 5/5, lesión hepática en 3/5, insuficiencia respiratoria en 3/5 y lesión miocardica en 2/5, 3 pacientes fueron tratados a base de pririmetamina más clindamicina o cotrimoxazol habiendo recuperación completa en 2 de ellos y uno fallecido con miocarditis por Toxoplasma gondii, 2 pacientes no recibieron tratamiento específico y la enfermedad se autolimitó sola; 4/5 tuvieron incrementos significativos de títulos (IFI) > 4 veces del valor basal ( rango: 4-250 veces); 3/5 tuvieron titulo + IgM (Elisa, IFI) y en 2/5 se detectó mediante biopsia la presencia del Toxoplasma gondii en el tejido pulmonar y miocárdico. Conclusión: Destacamos en forma importante la complicación oportunista de toxoplasmosis reactivada en pacientes con bartonellosis durante la fase aguda hemática. ( Rev Med Hered 1998; 9:14-20).
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