Skin hyperpigmentation following intravenous polymyxin B treatment associated with melanocyte activation and inflammatory process.

What is known and objective Polymyxins were widely used until the 1960s; however, they fell into disfavour owing to their toxicity. The subsequent growth of infections caused by multidrug-resistant Gram-negative bacteria has led to renewed use of this class of antimicrobials in clinical practice. Acquired skin hyperpigmentation (SH) following intravenous polymyxin B treatment has been previously reported, but little is known about its pathogenesis, clinical course and treatment. To improve understanding of these issues, we conducted a prospective study of adult patients receiving intravenous polymyxin B treatment. Methods Patients receiving intravenous polymyxin B treatment were followed throughout the course of treatment. Clinical, dermatoscopic, histologic and immunohistochemical skin properties of patients who presented with SH were studied. Results and discussion Skin hyperpigmentation was noted in 8% of patients (n=20/249); however, clinical, dermatoscopic, histologic and immunohistochemical examinations were performed only in three patients for whom the consent of relatives was obtained. Histologic and immunohistochemical findings showed an abundant melanocyte-pigmented dendritic network. Langerhans cells' hyperplasia and dermal IL-6 overexpression were also found, presumably for an inflammatory process due to polymyxin B use. As polymyxin B causes the release of histamine, which is known for its melanogenic effect, it is possible that skin darkening is associated with this inflammatory mediator. What is new These clinical and dermatoscopic findings contribute to a better understanding of how the pigmentary reaction manifests following intravenous polymyxin B treatment. Conclusion We concluded that hyperpigmentation due to intravenous polymyxin B treatment is associated with an inflammatory process and subsequent melanocyte activation. Although the pigmentary disorder neither influences the outcome of the therapy nor warrants discontinuation of treatment, it nevertheless considerably affects the patient's quality of life.

Association of Bartonella spp bacteremia with Chagas cardiomyopathy, endocarditis and arrythmias in patients from South America

Infection with Bartonella spp may cause cardiac arrhythmias, myocarditis and endocarditis in humans. The aim of the present study was to evaluate a possible association between Bartonella spp bacteremia and endocarditis, arrhythmia and Chagas cardiomyopathy in patients from Brazil and Argentina. We screened for the presence of bacterial 16S rRNA in human blood by PCR using oligonucleotides to amplify a 185-bp bacterial DNA fragment. Blood samples were taken from four groups of subjects in Brazil and Argentina: i) control patients without clinical disease, ii) patients with negative blood-culture endocarditis, iii) patients with arrhythmias, and iv) patients with chronic Chagas cardiomyopathy. PCR products were analyzed on 1.5% agarose gel to visualize the 185-bp fragment and then sequenced to confirm the identity of DNA. Sixty of 148 patients (40.5%) with cardiac disease and 1 of 56 subjects (1.8%) from the control group presented positive PCR amplification for Bartonella spp, suggesting a positive association of the bacteria with these diseases. Separate analysis of the four groups showed that the risk of a Brazilian patient with endocarditis being infected with Bartonella was 22 times higher than in the controls. In arrhythmic patients, the prevalence of infection was 45 times higher when compared to the same controls and 40 times higher for patients with Chagas cardiomyopathy. To the best of our knowledge this is the first report of the association between Bartonella spp bacteremia and Chagas disease. The present data may be useful for epidemiological and prevention studies in Brazil and Argentina.

Association of Bartonella spp bacteremia with Chagas cardiomyopathy, endocarditis and arrhythmias in patients from South America.

Infection with Bartonella spp may cause cardiac arrhythmias, myocarditis and endocarditis in humans. The aim of the present study was to evaluate a possible association between Bartonella spp bacteremia and endocarditis, arrhythmia and Chagas cardiomyopathy in patients from Brazil and Argentina. We screened for the presence of bacterial 16S rRNA in human blood by PCR using oligonucleotides to amplify a 185-bp bacterial DNA fragment. Blood samples were taken from four groups of subjects in Brazil and Argentina: i) control patients without clinical disease, ii) patients with negative blood-culture endocarditis, iii) patients with arrhythmias, and iv) patients with chronic Chagas cardiomyopathy. PCR products were analyzed on 1.5% agarose gel to visualize the 185-bp fragment and then sequenced to confirm the identity of DNA. Sixty of 148 patients (40.5%) with cardiac disease and 1 of 56 subjects (1.8%) from the control group presented positive PCR amplification for Bartonella spp, suggesting a positive association of the bacteria with these diseases. Separate analysis of the four groups showed that the risk of a Brazilian patient with endocarditis being infected with Bartonella was 22 times higher than in the controls. In arrhythmic patients, the prevalence of infection was 45 times higher when compared to the same controls and 40 times higher for patients with Chagas cardiomyopathy. To the best of our knowledge this is the first report of the association between Bartonella spp bacteremia and Chagas disease. The present data may be useful for epidemiological and prevention studies in Brazil and Argentina.

Bartonella henselae survives after the storage period of red blood cell units: is it transmissible by transfusion?

Bartonella henselae is the agent of cat scratch disease and bacillary angiomatosis. Blood donors can be asymptomatic carriers of B. henselae and the risk for transmission by transfusion should be considered. The objective of this study was to demonstrate that B. henselae remains viable in red blood cell (RBC) units at the end of the storage period. Two RBC units were split into two portions. One portion was inoculated with B. henselae and the other was used as a control. All units were stored at 4 degrees C for 35 days. Aliquots were collected on a weekly basis for culture in a dish with chocolate agar, ideal for the cultivation of this agent. Samples were collected on days 1 and 35 and taken for culture in Bact/Alert R blood culture bottles. Aliquots taken simultaneously were fixed in Karnovsky's medium for subsequent electron microscopy evaluation. Samples from infected bags successfully isolated B. henselae by chocolate agar culture, although Bact/Alert R blood culture bottles remained negative. Bartonella spp. structures within erythrocytes were confirmed by electron microscopy. The viability of B. henselae was demonstrated after a storage period of RBC units. These data reinforce the possibility of infection by transfusion of blood units collected from asymptomatic blood donors.

Treatment of human papillomavirus with peg-interferon alfa-2b and ribavirin.

We reported one case of human immunodeficiency virus and hepatitis C virus co-infected patient who presented a significant improvement of human papillomavirus (HPV) lesions during the treatment of chronic hepatitis using peg-interferon alfa-2b and ribavirin.

Treatment of human papillomavirus with peg-interferon alfa-2b and ribavirin

We reported one case of human immunodeficiency virus and hepatitis C virus co-infected patient who presented a significant improvement of human papillomavirus (HPV) lesions during the treatment of chronic hepatitis using peg-interferon alfa-2b and ribavirin.

Pyoderma gangrenosum as first clinical manifestation of gastric adenocarcinoma.

Pyoderma gangrenosum (PG) is a neutrophilic dermatosis of unknown etiology characterized by typical skin ulcers. It may be related to systemic disorders but its association with solid tumors is very unusual. In this setting, we describe a patient in whom PG was the first and isolated manifestation of advanced gastric adenocarcinoma.

Baccilary angiomatosis: negative results using normal Balb/c and Balb/c nude mice

Baccilary angiomatosis has recently been described as a disease that can spread systematically and that is potentially fatal. It is caused by Bartonella henselae and B. quintana, and presents as especially pronounced signs and symptoms in patients suffering from acquired immunodeficiency syndrome (AIDS). To clarify the pathogenesis of the disease and to try to define the relationships among baccilary angiomatosis, cat scratch disease and Carrión's bartonellosis, the authors of this study have attempted to develop an experimental model using mice that were immunocompetent as well as those that had their cellular immunity genetically compromised. A know concentration of B. henselae was inoculated intradermally in Balb/c an isogenic mice or an athymic group of the same lineage. Blood samples were taken on days-0, 3, 7, 10, 14, 28, and 60 after inoculation for indirect immunofluorescence antibody testing. On the 21st and 60th day, one animal from each group was sacrificed and a post mortem carried out including histological evaluation of the liver, spleen, lymph nodes, skin and other organs. Hemocultures of the sacrificed animals were collected. All results of serologic response, cultures and histologic examination were negative. The authors discuss the methodology, especially the use of isogenic animals of the same lineage in B. henselae infection, with and without immunodeficiency, and the resources for the negative results of histopathology, serology and cultures.

Decreased reduced glutathione and glutathione reductase activity in subjects with hemoglobin C.

Erythrocyte catalase, reduced glutathione, glutathione peroxidase and glutathione reductase were determined in 17 normal black controls, 8 subjects with Hb AC, 12 with Hb SC, 1 with Hb CC and 18 patients with sickle cell anemia. Catalase and glutathione peroxidase activities were decreased in sickle cell anemia. Reduced glutathione and glutathione reductase activity were significantly lower in subjects with Hb C (AC, CC, SC). Differences were observed between Hb C, Hb S and Hb A as regards red cell dehydration, intracellular crystallization, enhanced potassium efflux, an increased number of titratable SH groups in Hb C and the binding of Hb C to band 3 on the inner membrane surface. A decrease in reduced glutathione, probably due to inhibition or decreased synthesis of glutathione reductase, was also observed. All these factors may determine oxidation of Hb C, possibly contributing to the hemolysis in patients with Hb C disease.