Levofloxacin Treatment Failure In Haemophilus Influenzae Pneumonia

We describe the first case of failure of oral levofloxacin treatment of community-acquired pneumonia caused by Haemophilus influenzae. The strain showed cross-resistance to fluoroquinolones and carried four mutations in quinolone resistance-determining regions of DNA gyrase and topoisomerase IV genes

Immunosuppression and Chagas disease: a management challenge

Immunosuppression, which has become an increasingly relevant clinical condition in the last 50 years, modifies the natural history of Trypanosoma cruzi infection in most patients with Chagas disease. The main goal in this setting is to prevent the consequences of reactivation of T. cruzi infection by close monitoring. We analyze the relationship between Chagas disease and three immunosuppressant conditions, including a description of clinical cases seen at our center, a brief review of the literature, and recommendations for the management of these patients based on our experience and on the data in the literature. T. cruzi infection is considered an opportunistic parasitic infection indicative of AIDS, and clinical manifestations of reactivation are more severe than in acute Chagas disease. Parasitemia is the most important defining feature of reactivation. Treatment with benznidazole and/or nifurtimox is strongly recommended in such cases. It seems reasonable to administer trypanocidal treatment only to asymptomatic immunosuppressed patients with detectable parasitemia, and/or patients with clinically defined reactivation. Specific treatment for Chagas disease does not appear to be related to a higher incidence of neoplasms, and a direct role of T. cruzi in the etiology of neoplastic disease has not been confirmed. Systemic immunosuppressive diseases or immunosuppressants can modify the natural course of T. cruzi infection. Immunosuppressive doses of corticosteroids have not been associated with higher rates of reactivation of Chagas disease. Despite a lack of evidence-based data, treatment with benznidazole or nifurtimox should be initiated before immunosuppression where possible to reduce the risk of reactivation. Timely antiparasitic treatment with benznidazole and nifurtimox (or with posaconazole in cases of therapeutic failure) has proven to be highly effective in preventing Chagas disease reactivation, even if such treatment has not been formally incorporated into management protocols for immunosuppressed patients. International consensus guidelines based on expert opinion would greatly contribute to standardizing the management of immunosuppressed patients with Chagas disease

Levofloxacin Treatment Failure In Haemophilus Influenzae Pneumonia

We describe the first case of failure of oral levofloxacin treatment of community-acquired pneumonia caused by Haemophilus influenzae. The strain showed cross-resistance to fluoroquinolones and carried four mutations in quinolone resistance-determining regions of DNA gyrase and topoisomerase IV genes

Immunosuppression and Chagas disease: a management challenge

Immunosuppression, which has become an increasingly relevant clinical condition in the last 50 years, modifies the natural history of Trypanosoma cruzi infection in most patients with Chagas disease. The main goal in this setting is to prevent the consequences of reactivation of T. cruzi infection by close monitoring. We analyze the relationship between Chagas disease and three immunosuppressant conditions, including a description of clinical cases seen at our center, a brief review of the literature, and recommendations for the management of these patients based on our experience and on the data in the literature. T. cruzi infection is considered an opportunistic parasitic infection indicative of AIDS, and clinical manifestations of reactivation are more severe than in acute Chagas disease. Parasitemia is the most important defining feature of reactivation. Treatment with benznidazole and/or nifurtimox is strongly recommended in such cases. It seems reasonable to administer trypanocidal treatment only to asymptomatic immunosuppressed patients with detectable parasitemia, and/or patients with clinically defined reactivation. Specific treatment for Chagas disease does not appear to be related to a higher incidence of neoplasms, and a direct role of T. cruzi in the etiology of neoplastic disease has not been confirmed. Systemic immunosuppressive diseases or immunosuppressants can modify the natural course of T. cruzi infection. Immunosuppressive doses of corticosteroids have not been associated with higher rates of reactivation of Chagas disease. Despite a lack of evidence-based data, treatment with benznidazole or nifurtimox should be initiated before immunosuppression where possible to reduce the risk of reactivation. Timely antiparasitic treatment with benznidazole and nifurtimox (or with posaconazole in cases of therapeutic failure) has proven to be highly effective in preventing Chagas disease reactivation, even if such treatment has not been formally incorporated into management protocols for immunosuppressed patients. International consensus guidelines based on expert opinion would greatly contribute to standardizing the management of immunosuppressed patients with Chagas disease

Immunosuppression and Chagas disease: a management challenge

Immunosuppression, which has become an increasingly relevant clinical condition in the last 50 years, modifies the natural history of Trypanosoma cruzi infection in most patients with Chagas disease. The main goal in this setting is to prevent the consequences of reactivation of T. cruzi infection by close monitoring. We analyze the relationship between Chagas disease and three immunosuppressant conditions, including a description of clinical cases seen at our center, a brief review of the literature, and recommendations for the management of these patients based on our experience and on the data in the literature. T. cruzi infection is considered an opportunistic parasitic infection indicative of AIDS, and clinical manifestations of reactivation are more severe than in acute Chagas disease. Parasitemia is the most important defining feature of reactivation. Treatment with benznidazole and/or nifurtimox is strongly recommended in such cases. It seems reasonable to administer trypanocidal treatment only to asymptomatic immunosuppressed patients with detectable parasitemia, and/or patients with clinically defined reactivation. Specific treatment for Chagas disease does not appear to be related to a higher incidence of neoplasms, and a direct role of T. cruzi in the etiology of neoplastic disease has not been confirmed. Systemic immunosuppressive diseases or immunosuppressants can modify the natural course of T. cruzi infection. Immunosuppressive doses of corticosteroids have not been associated with higher rates of reactivation of Chagas disease. Despite a lack of evidence-based data, treatment with benznidazole or nifurtimox should be initiated before immunosuppression where possible to reduce the risk of reactivation. Timely antiparasitic treatment with benznidazole and nifurtimox (or with posaconazole in cases of therapeutic failure) has proven to be highly effective in preventing Chagas disease reactivation, even if such treatment has not been formally incorporated into management protocols for immunosuppressed patients. International consensus guidelines based on expert opinion would greatly contribute to standardizing the management of immunosuppressed patients with Chagas disease

Patients with Chagas disease and HIV infection: demographic and clinical manifestations related to Chagas disease

a<p>Mild chronic cardiac disease according to Kuschnir classification <a href="http://www.plosntds.org/article/info:doi/10.1371/journal.pntd.0001965#pntd.0001965-Kuschnir1" target="_blank">[67]</a>.</p>b<p>Relevant comorbidities: asymptomatic strongyloidosis diagnosed in 2006 treated with albendazole and ivermectin; type 2 diabetes mellitus and high blood pressure, well controlled by oral antidiabetic and antihypertensive drugs; macrocytic anemia due to folic acid deficiency.</p><p>VC, contact with vector; VT, mother with <i>T. cruzi</i> infection; TF, transfusion in endemic area; BZD, benznidazole; CCC, chronic cardiac disease stage; ND, no data; NA, not accomplished.</p

Demographic and clinical manifestations of patients with <i>T. cruzi</i> infection and neoplastic disease.

a<p>Severe chronic cardiac disease according to Kuschnir classification.</p><p>ND, no data; NA, not accomplished; NR, no reactivations; VC, contact with the vector; VT, mother with <i>T. cruzi</i> infection; IND, indeterminate stage of Chagas disease; CCC, chronic cardiac disease stage; R-MEGACHOP, Rituximab-MEGACHOP; R-ESHAP, Rituximab-ESHAP; IDICE-G, idarubicin, ARA-C, etoposide; MTX, intrathecal methotrexate; Mitox, mitoxantrone; VBCMP or M2, vincristine, carmustine, melphalan, cyclophosphamide, prednisone; LN: lymph node.</p

Patients with systemic autoimmune diseases: demographic and clinical manifestations related to autoimmune disease

<p>AM, acid mycophenolic; AZA, azathioprine; CYC, cyclophosphamide; HDX, hydroxychloroquine; MP, methylprednisolone; PDN, prednisone; RA, rheumatoid arthritis; SLE, systemic lupus erythematosus.</p

Patients with systemic autoimmune diseases: demographic and clinical manifestations related to Chagas disease

a<p>Mild chronic cardiac disease according to Kuschnir classification <a href="http://www.plosntds.org/article/info:doi/10.1371/journal.pntd.0001965#pntd.0001965-Kuschnir1" target="_blank">[67]</a>.</p>b<p>PCR was negative in nine determinations between 03/18/2008 and 07/02/2010, after treatment with posaconazole.</p><p>VC, contact with the vector; TF, transfusion in endemic area; BZD, Benznidazole; CCC, chronic cardiac disease stage; ND, no data.</p