Epidemiological profile, spatial patterns and priority areas for surveillance and control of leishmaniasis in Brazilian border strip, 2009-2017.

Leishmaniasis represents a major neglected public health problem and the control measures have not been successful in Brazil. Recent studies have shown leishmaniasis importance to Brazilian border zones which reinforces the need to investigate its spread in those regions. This study aimed to analyze epidemiologic profile and its spatial distribution or aggregation process in both tegumentary and visceral leishmaniasis in the Brazilian border strip from 2009 to 2017. This is an ecological study of the epidemiological profile and spatial patterns encompassing municipalities in the Brazilian border strip. The presence of spatial autocorrelation and determination of priority areas for disease control were performed using global (Moran I) and local (LISA) Moran spatial techniques. The annual mean coefficients of tegumentary and visceral leishmaniasis were 29.8 and 0.6 by 100,000 inhabitants in the border strip, respectively. The indigenous population rates of leishmaniasis in the border zone appears to be higher than in the rest of the country (cutaneous changed from 33.2% to 6.6% and visceral rising from 1.0% to 17.5%) in the period. The most affected municipalities were located in the North and Central arches of the border zone. The results can subsidize the development of more targeted and effective strategies that can contribute to the surveillance and control of leishmaniasis in border zones, as the provision of epidemiological and spatial data on the disease. For better control of the disease, we recommend and emphasize the need to integrate public health policies of neighboring countries.

Osteopontin Is Upregulated in Human and Murine Acute Schistosomiasis Mansoni.

BACKGROUND: Symptomatic acute schistosomiasis mansoni is a systemic hypersensitivity reaction against the migrating schistosomula and mature eggs after a primary infection. The mechanisms involved in the pathogenesis of acute schistosomiasis are not fully elucidated. Osteopontin has been implicated in granulomatous reactions and in acute hepatic injury. Our aims were to evaluate if osteopontin plays a role in acute Schistosoma mansoni infection in both human and experimentally infected mice and if circulating OPN levels could be a novel biomarker of this infection. METHODOLOGY/PRINCIPAL FINDINGS: Serum/plasma osteopontin levels were measured by ELISA in patients with acute (n = 28), hepatointestinal (n = 26), hepatosplenic (n = 39) schistosomiasis and in uninfected controls (n = 21). Liver osteopontin was assessed by immunohistochemistry in needle biopsies of 5 patients. Sera and hepatic osteopontin were quantified in the murine model of schistosomiasis mansoni during acute (7 and 8 weeks post infection, n = 10) and chronic (30 weeks post infection, n = 8) phase. Circulating osteopontin levels are increased in patients with acute schistosomiasis (p = 0.0001). The highest levels of OPN were observed during the peak of clinical symptoms (7-11 weeks post infection), returning to baseline level once the granulomas were modulated (>12 weeks post infection). The plasma levels in acute schistosomiasis were even higher than in hepatosplenic patients. The murine model mirrored the human disease. Macrophages were the major source of OPN in human and murine acute schistosomiasis, while the ductular reaction maintains OPN production in hepatosplenic disease. Soluble egg antigens from S. mansoni induced OPN expression in primary human kupffer cells. CONCLUSIONS/SIGNIFICANCE: S. mansoni egg antigens induce the production of OPN by macrophages in the necrotic-exudative granulomas characteristic of acute schistosomiasis mansoni. Circulating OPN levels are upregulated in human and murine acute schistosomiasis and could be a non-invasive biomarker of this form of disease.

Correction: Vestibular Evoked Myogenic Potential (VEMP) Triggered by Galvanic Vestibular Stimulation (GVS): A Promising Tool to Assess Spinal Cord Function in Schistosomal Myeloradiculopathy.

[This corrects the article DOI: 10.1371/journal.pntd.0004672.].