Plasmodium falciparum malaria and Parvovirus B19; a case of acute co-infection

<p>Abstract</p> <p>Background</p> <p>Co-infection with Plasmodium falciparum malaria and Parvovirus B19 in adults is an extremely rare occurrence and, apparently, only one case has been previously reported. Herein we describe a case of acute co-infection with severe anemia and renal failure.</p> <p>Case presentation</p> <p>The patient was a 34-year-old African man presenting myalgia, fatigue, headache, anemia and hepatosplenomegaly. A thin peripheral smear showed Plasmodium falciparum trophozoites and the patient was treated with oral mefloquine. After an initial amelioration, fever, fatigue and myalgia reappeared, the anemia worsened and there was evidence of acute renal failure. No malarial parasites were found with a blood smear. A bone marrow aspiration showed marked erythroid hypoplasia. Parvovirus B19-specific IgM and IgG and viremia were positive. The patient was treated with steroids and blood cell transfusions. After ten days, anemia and renal failure progressively decreased. When last seen, the patient was asymptomatic and the blood values were within the normal range.</p> <p>Conclusions</p> <p>The diagnosis of Parvovirus B19 acute infection should be considered in any case of persistent severe anemia and/or renal failure, even in clinical conditions that are well-known causes of anemia and renal failure, such as malaria.</p

Circulating Microbial Products and Acute Phase Proteins as Markers of Pathogenesis in Lymphatic Filarial Disease

Lymphatic filariasis can be associated with development of serious pathology in the form of lymphedema, hydrocele, and elephantiasis in a subset of infected patients. Dysregulated host inflammatory responses leading to systemic immune activation are thought to play a central role in filarial disease pathogenesis. We measured the plasma levels of microbial translocation markers, acute phase proteins, and inflammatory cytokines in individuals with chronic filarial pathology with (CP Ag+) or without (CP Ag−) active infection; with clinically asymptomatic infections (INF); and in those without infection (endemic normal [EN]). Comparisons between the two actively infected groups (CP Ag+ compared to INF) and those without active infection (CP Ag− compared to EN) were used preliminarily to identify markers of pathogenesis. Thereafter, we tested for group effects among all the four groups using linear models on the log transformed responses of the markers. Our data suggest that circulating levels of microbial translocation products (lipopolysaccharide and LPS-binding protein), acute phase proteins (haptoglobin and serum amyloid protein-A), and inflammatory cytokines (IL-1β, IL-12, and TNF-α) are associated with pathogenesis of disease in lymphatic filarial infection and implicate an important role for circulating microbial products and acute phase proteins

Schistosoma mansoni Enhances Host Susceptibility to Mucosal but Not Intravenous Challenge by R5 Clade C SHIV

Parasitic infections have been postulated to increase host susceptibility to HIV-1. We previously demonstrated that rhesus monkeys with active schistosomiasis were significantly more likely to become systemically infected after intrarectal exposure to an R5-tropic clade C simian-human immunodeficiency virus then were parasite-free control animals. However, we could not address whether parasites exert their effect at the mucosal level or systemically. To address the latter possibility, we measured the virus doses needed to achieve systemic infection after intravenous exposure of parasite-free or parasite-positive monkeys using the identical virus stock. None of the viral parameters tested in these two groups of monkeys were statistically significantly different. These results suggest that schistosomiasis modulates susceptibility to immunodeficiency virus acquisition predominantly at the mucosal level. Treatment for parasitic infections in populations at higher risk for HIV-1 acquisition could represent a cost-effective approach to slow the spread of HIV-1, which is predominantly transmitted through mucosal routes

Recent advances in understanding Cushing disease: resistance to glucocorticoid negative feedback and somatic USP8 mutations

Cushing’s disease is a rare disease with a characteristic phenotype due to significant hypercortisolism driven by over-secretion of adrenocorticotropic hormone and to high morbidity and mortality if untreated. It is caused by a corticotroph adenoma of the pituitary, but the exact mechanisms leading to tumorigenesis are not clear. Recent advances in molecular biology such as the discovery of somatic mutations of the ubiquitin-specific peptidase 8 (USP8) gene allow new insights into the pathogenesis, which could be translated into exciting and much-needed therapeutic applications

A Family of Helminth Molecules that Modulate Innate Cell Responses via Molecular Mimicry of Host Antimicrobial Peptides

Over the last decade a significant number of studies have highlighted the central role of host antimicrobial (or defence) peptides in modulating the response of innate immune cells to pathogen-associated ligands. In humans, the most widely studied antimicrobial peptide is LL-37, a 37-residue peptide containing an amphipathic helix that is released via proteolytic cleavage of the precursor protein CAP18. Owing to its ability to protect against lethal endotoxaemia and clinically-relevant bacterial infections, LL-37 and its derivatives are seen as attractive candidates for anti-sepsis therapies. We have identified a novel family of molecules secreted by parasitic helminths (helminth defence molecules; HDMs) that exhibit similar biochemical and functional characteristics to human defence peptides, particularly CAP18. The HDM secreted by Fasciola hepatica (FhHDM-1) adopts a predominantly α-helical structure in solution. Processing of FhHDM-1 by F. hepatica cathepsin L1 releases a 34-residue C-terminal fragment containing a conserved amphipathic helix. This is analogous to the proteolytic processing of CAP18 to release LL-37, which modulates innate cell activation by classical toll-like receptor (TLR) ligands such as lipopolysaccharide (LPS). We show that full-length recombinant FhHDM-1 and a peptide analogue of the amphipathic C-terminus bind directly to LPS in a concentration-dependent manner, reducing its interaction with both LPS-binding protein (LBP) and the surface of macrophages. Furthermore, FhHDM-1 and the amphipathic C-terminal peptide protect mice against LPS-induced inflammation by significantly reducing the release of inflammatory mediators from macrophages. We propose that HDMs, by mimicking the function of host defence peptides, represent a novel family of innate cell modulators with therapeutic potential in anti-sepsis treatments and prevention of inflammation

Community-Acquired Acute Bacterial Meningitis In The Elderly In Turkey

P>This investigation aimed both to delineate the current status of community-acquired acute bacterial meningitis and to produce data on the interrelationships between clinical, laboratory and therapeutic parameters in the elderly. This retrospective cohort study was conducted in 28 Turkish institutions in 159 culture-positive patients over the age of 50 years. Streptococcus pneumoniae was the most common pathogen (69.2%), followed by Listeria monocytogenes (8.8%). For this reason, antilisterial antibiotics such as ampicillin or benzylpenicillin should be added to the therapeutic regimen. Pathogen-specific mortality did not vary between S. pneumoniae and L. monocytogenes. The overall mortality was 2.5% at the third day, 12.6% at the seventh day, 20.1% at the 14th day and 21.4% at the 21st day. The risk factors for fatality were increasing age, the presence of stupor, sepsis and inappropriate antibiotic administration. Cerebrospinal fluid (CSF) leukocyte counts and CSF/blood glucose ratios were lower in patients who died. Fever did not differ between survivors and fatal cases. The mean duration of antibiotic therapy in survivors was 16.3 +/- 6.4 days. One-fifth of the patients had complications, and in 5.7% of the patients sequelae persisted at follow-up.WoSScopu

Learning SVM from Distributed, Non-Linearly Separable Datasets with Kernel Methods

Learning from distributed data sets is common problem nowadays and the question of its actuality can be inferred by the number of applications and from even higher number of problems coming from real world business solutions. Here we will review the question of distributed classification with Support Vector Machines, and present our approach to handle the problem in effective way

Evaluation of geriatric infections in past six years

WOS: 000440345100505

Metastatic prolactinoma: case report with immunohistochemical assessment for p53 and Ki-67 antigens Prolactinoma metastático: relato de caso com avaliação imuno-histoquímica para os antígenos p53 e Ki-67

Pituitary carcinomas are rare neoplasms characterized by craniospinal and/or systemic metastases originated from the pituitary. Their histopathology is frequently indistinguishable from that of benign adenomas. The development of markers that better reflect their behavior is desirable. We present the case of a 47 year-old man with a prolactin-secreting macroadenoma who was submitted to surgeries, cranial radiation therapy, and bromocriptine treatment, but evolved to a fatal outcome after the disclosure of intracranial metastases. Tumor samples underwent p53 and Ki-67 immunohistochemical assessment. p53 was absent in all samples, a rare finding among pituitary carcinomas. Ki-67 proliferative index was 2.80% in the original tumor, 4.40% in the relapse, and 4.45% in the metastasis. The figure in the relapse is higher than the expected for a noninvasive adenoma. In conclusion, p53 staining is not positive in all pituitary carcinomas. A high Ki-67 proliferative index in a pituitary adenoma might indicate a more aggressive behavior.<br>Carcinomas pituitários são neoplasias raras caracterizadas pela presença de metástases cranio-espinhais e/ou sistêmicas originadas da hipófise. Sua histopatologia é freqüentemente indistinguível daquela dos adenomas benignos. O desenvolvimento de marcadores que melhor reflitam o seu comportamento é desejável. Apresentamos o caso de um homem de 47 anos com um macroadenoma secretor de prolactina que foi submetido a procedimentos cirúrgicos, radioterapia e tratamento com bromocriptina, mas que evoluiu para o óbito após o descobrimento de metástases intracranianas. Amostras do tumor foram submetidas à análise imuno-histoquímica para os antígenos p53 e Ki-67. A coloração para p53 foi negativa em todas as amostras, um achado raro entre os carcinomas pituitários. O índice proliferativo Ki-67 foi 2,80% no tumor original, 4,40% na recidiva e 4,45% na metástase. O valor obtido na recidiva é maior que o esperado para um adenoma não-invasor. Concluindo, a coloração para p53 não é positiva em todos os carcinomas pituitários. Um índice proliferativo Ki-67 alto em um adenoma pituitário poderia indicar um comportamento mais agressivo