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1.
The lancet ; 388(16): 898-904, 2016.
Article in English | Sec. Est. Saúde SP, LILACS | ID: biblio-1024191

ABSTRACT

Zika virus is an arthropod-borne virus that is a member of the family Flaviviridae transmitted mainly by mosquitoes of the genus Aedes. Although usually asymptomatic, infection can result in a mild and self-limiting illness characterised by fever, rash, arthralgia, and conjunctivitis. An increase in the number of children born with microcephaly was noted in 2015 in regions of Brazil with high transmission of Zika virus. More recently, evidence has been accumulating supporting a link between Zika virus and microcephaly. Here, we describe findings from three fatal cases and two spontaneous abortions associated with Zika virus infection.


Subject(s)
Child , Zika Virus , Microcephaly
2.
Ticks Tick Borne Dis ; 6(5): 649-52, 2015 Jul.
Article in English | MEDLINE | ID: mdl-26123434

ABSTRACT

Babesiosis, an infection caused by the protozoan Babesia microti and transmitted by the Ixodes scapularis tick, is commonly described in the literature with an approximate incidence of 1000 cases per year (Herwaldt et al., 2012). Infections in North America occur most frequently during the spring and summer months in the Northeastern and Midwestern United States. Babesia can cause a wide spectrum of clinical manifestations ranging from a self-limited febrile illness or mild anemia to severe illness causing acute respiratory distress syndrome (ARDS), disseminated intravascular coagulopathy (DIC) and multisystem organ failure. Severe illness most commonly occurs in elderly, immunocompromised, or asplenic patients (Vannier and Krause, 2012). Splenic rupture has been generally described as a complication of severe illness secondary to babesiosis. We describe a case of spontaneous splenic rupture in an otherwise healthy woman that required emergent splenectomy. Recent case reports suggest that splenic rupture occurs in people without known risk factors for severe babesiosis. Physicians should be aware of this acute presentation in otherwise healthy individuals.


Subject(s)
Babesiosis/complications , Rupture, Spontaneous/parasitology , Splenic Diseases/etiology , Splenic Diseases/pathology , Animals , Azithromycin/administration & dosage , Azithromycin/therapeutic use , Babesia/isolation & purification , Babesiosis/drug therapy , Doxycycline/administration & dosage , Doxycycline/therapeutic use , Hematoma/etiology , Hematoma/pathology , Hemoperitoneum/etiology , Hemoperitoneum/pathology , Humans , Middle Aged , Splenectomy , Splenic Diseases/surgery
3.
Proc Natl Acad Sci U S A ; 106(22): 9027-32, 2009 Jun 02.
Article in English | MEDLINE | ID: mdl-19451638

ABSTRACT

Intermittent preventive treatment in pregnancy (IPTp) is used to prevent Plasmodium falciparum malaria. However, parasites resistant to the IPTp drug sulfadoxine-pyrimethamine (SP) have emerged worldwide, and infections with mixed resistant and susceptible parasites are exacerbated by pyrimethamine in mice. In a prospective delivery cohort in Muheza, Tanzania, we examined the effects of SP IPTp on parasite resistance alleles, parasite diversity, level of parasitemia, and inflammation in the placenta. IPTp use was associated with an increased fraction of parasites carrying the resistance allele at DHPS codon 581, an increase in the level of parasitemia, and more intense placental inflammation. The lowest mean level of parasite diversity and highest mean level of parasitemia occurred in women after recent IPTp use. These findings support a model of parasite release and facilitation, whereby the most highly resistant parasites out-compete less fit parasite populations and overgrow under drug pressure. Use of partially effective anti-malarial agents for IPTp may exacerbate malaria infections in the setting of widespread drug resistance.


Subject(s)
Antimalarials/administration & dosage , Drug Resistance , Malaria, Falciparum/prevention & control , Plasmodium falciparum/genetics , Pregnancy Complications, Parasitic/prevention & control , Pyrimethamine/administration & dosage , Sulfadoxine/administration & dosage , Adult , Alleles , Animals , Cohort Studies , Dihydropteroate Synthase/genetics , Drug Combinations , Female , Humans , Malaria, Falciparum/parasitology , Mice , Plasmodium falciparum/drug effects , Plasmodium falciparum/isolation & purification , Pregnancy , Pregnancy Complications, Parasitic/parasitology , Prospective Studies , Selection, Genetic , Tanzania , Tetrahydrofolate Dehydrogenase/genetics , Young Adult
4.
Ultrastruct Pathol ; 23(5): 285-97, 1999.
Article in English | MEDLINE | ID: mdl-10582266

ABSTRACT

Crystalloid inclusions or "pole bodies" observed in brain macrophages in human demyelinating disease represent a morphological enigma. Similar inclusions were detected in brain macrophages from the GFAP-IL3 mouse, a transgenic murine model for macrophage mediated demyelination. Mice also showed inclusions in hematopoietic tissue. They appear to be related to phagocytosis and secretion, respectively, as evidenced by the fact that in phagocytosing cells they often merged with lysozomes and that affected cells showed empty channels open to the interstitium. Based on ultrastructural and immunolocalization studies using chaperonin-10, lysozyme, and cathepsin the authors suggest that these inclusions are consistent with phagocytosis-related secretory products. This study may provide insight into the nature and significance of similar macrophage inclusions recently identified in multiple sclerosis.


Subject(s)
Bone Marrow Cells/ultrastructure , Cerebellum/pathology , Glial Fibrillary Acidic Protein/biosynthesis , Inclusion Bodies/ultrastructure , Interleukin-3/biosynthesis , Macrophages/ultrastructure , Multiple Sclerosis/pathology , Animals , Bone Marrow Cells/metabolism , Cathepsins/metabolism , Cerebellum/metabolism , Chaperonin 10/metabolism , Crystallization , Disease Models, Animal , Glial Fibrillary Acidic Protein/genetics , Inclusion Bodies/metabolism , Interleukin-3/genetics , Macrophages/metabolism , Mice , Mice, Transgenic , Multiple Sclerosis/etiology , Multiple Sclerosis/metabolism , Muramidase/metabolism
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