﻿<?xml version="1.0" encoding="utf-8"?><rss version="2.0"><channel><title>Interdisciplinary Perspectives on Infectious Diseases</title><link>http://www.hindawi.com</link><description>The latest articles from Hindawi Publishing Corporation</description><copyright>&amp;#169; 2010, Hindawi Publishing Corporation. All rights reserved.</copyright><item><title>Enteroaggregative Escherichia coli: An Emerging Enteric Food Borne Pathogen</title><link>http://www.hindawi.com/journals/ipid/2010/254159.html</link><description>Enteroaggregative Escherichia coli (EAEC) are quite heterogeneous category of an emerging enteric pathogen associated with cases of acute or persistent diarrhea worldwide in children and adults, and over the past decade has received increasing attention as a cause of watery diarrhea, which is often persistent. EAEC infection is an important cause of diarrhea in outbreak and non-outbreak settings in developing and developed countries. Recently, EAEC has been implicated in the development of irritable bowel syndrome, but this remains to be confirmed. EAEC is defined as a diarrheal pathogen based on its characteristic aggregative adherence (AA) to HEp-2 cells in culture and its biofilm formation on the intestinal mucosa with a &amp;#8220;stacked-brick&amp;#8221; adherence phenotype, which is related to the presence of a 60 MDa plasmid (pAA). At the molecular level, strains demonstrating the aggregative phenotype are quite heterogeneous; several virulence factors are detected by polymerase chain reaction; however, none exhibited 100&amp;#37; specificity. Although several studies have identified specific virulence factor(s) unique to EAEC, the mechanism by which EAEC exerts its pathogenesis is, thus, far unknown. The present review updates the current knowledge on the epidemiology, chronic complications, detection, virulence factors, and treatment of EAEC, an emerging enteric food borne pathogen.</description><Author>P. Kaur, A. Chakraborti, and A. Asea</Author><copyright>&amp;#169; 2010, Hindawi Publishing Corporation. All rights reserved.</copyright></item><item><title>Rhombencephalitis Caused by Listeria monocytogenes in Humans and Ruminants: A Zoonosis on the Rise?</title><link>http://www.hindawi.com/journals/ipid/2010/632513.html</link><description>Listeriosis is an emerging zoonotic infection of humans and ruminants worldwide caused by Listeria monocytogenes (LM). In both host species, CNS disease accounts for the high mortality associated with listeriosis and includes rhombencephalitis, whose neuropathology is strikingly similar in humans and ruminants. This review discusses the current knowledge about listeric encephalitis, and involved host and bacterial factors. There is an urgent need to study the molecular mechanisms of neuropathogenesis, which are poorly understood. Such studies will provide a basis for the development of new therapeutic strategies that aim to prevent LM from invading the brain and spread within the CNS.</description><Author>Anna Oevermann, Andreas Zurbriggen, and Marc Vandevelde</Author><copyright>&amp;#169; 2010, Hindawi Publishing Corporation. All rights reserved.</copyright></item><item><title>Animal Models of CNS Viral Disease: Examples from Borna Disease Virus Models</title><link>http://www.hindawi.com/journals/ipid/2010/709791.html</link><description>Borna disease (BD), 
                  caused by the neurotropic RNA virus, Borna 
                  Disease virus, is an affliction ranging from 
                  asymptomatic to fatal meningoencephalitis across 
                  naturally and experimentally infected 
                  warmblooded (mammalian and bird) species.  More 
                  than 100 years after the first clinical 
                  descriptions of Borna disease in horses and 
                  studies beginning in the 1980&amp;#39;s linking 
                  Borna disease virus to human neuropsychiatric 
                  diseases, experimentally infected rodents have 
                  been used as models for examining behavioral, 
                  neuropharmacological, and neurochemical responses 
                  to viral challenge at different stages of life. 
                  These studies have contributed to understanding 
                  the role of CNS viral injury in vulnerability to 
                  behavioral, developmental, epileptic, and 
                  neurodegenerative diseases and aided evaluation 
                  of the proposed and still controversial links to 
                  human disease.</description><Author>Marylou V. Solbrig</Author><copyright>&amp;#169; 2010, Hindawi Publishing Corporation. All rights reserved.</copyright></item><item><title>Chlamydophila pneumoniae Infection and Its Role in Neurological Disorders</title><link>http://www.hindawi.com/journals/ipid/2010/273573.html</link><description>Chlamydophila pneumoniae is an intracellular pathogen responsible for a number of different acute and chronic infections. The recent deepening of knowledge on the biology and the use of increasingly more sensitive and
specific molecular techniques has allowed demonstration of C. pneumoniae in
a large number of persons suffering from different diseases including cardiovascular (atherosclerosis and stroke) and central nervous system (CNS) disorders. Despite this, many important issues remain unanswered with regard to the role that C. pneumoniae may play in initiating atheroma or in the progression of the disease. A growing body of evidence concerns the involvement of this pathogen in chronic neurological disorders and particularly in Alzheimer&amp;#39;s disease (AD) and Multiple Sclerosis (MS). Monocytes may traffic C. pneumoniae across the blood-brain-barrier, shed the organism in the
CNS and induce neuroinflammation. The demonstration of C. pneumoniae by
histopathological, molecular and culture techniques in the late-onset AD dementia has suggested a relationship between CNS infection with C. pneumoniae and the AD neuropathogenesis. In particular subsets of MS patients, C. pneumoniae could induce a chronic persistent brain infection acting as a cofactor in the development of the disease. The role of Chlamydia in the pathogenesis of mental or neurobehavioral disorders including schizophrenia and autism is uncertain and fragmentary and will require further
confirmation.</description><Author>Carlo Contini, Silva Seraceni, Rosario Cultrera, Massimiliano Castellazzi, Enrico Granieri, and Enrico Fainardi</Author><copyright>&amp;#169; 2010, Hindawi Publishing Corporation. All rights reserved.</copyright></item><item><title>Biogeography of Tick-Borne Bhanja Virus (Bunyaviridae) in Europe</title><link>http://www.hindawi.com/journals/ipid/2009/372691.html</link><description>Bhanja virus (BHAV) is pathogenic for young domestic ruminants and also for humans, causing fever and affections of the central nervous system. This generally neglected arbovirus of the family Bunyaviridae is transmitted by metastriate ticks of the genera Haemaphysalis, Dermacentor, Hyalomma, Rhipicephalus, Boophilus, and Amblyomma. Geographic distribution of BHAV covers southern and Central Asia, Africa, and southern (partially also central) Europe. Comparative biogeographic study of eight known natural foci of BHAV infections in Europe (in Italy, Croatia, Bulgaria, Slovakia) has revealed their common features.  (1) submediterranean climatic pattern with dry growing season and wet mild winter (or microlimatically similar conditions, e.g., limestone karst areas in central Europe), (2) xerothermic woodland-grassland ecosystem, with plant alliances Quercetalia pubescentis, Festucetalia valesiacae, and Brometalia erecti, involving pastoral areas, (3) presence of at least one of the tick species Haemaphysalis punctata, Dermacentor marginatus, Rhipicephalus bursa, and/or Hyalomma marginatum, and (4) presence of &amp;#x2265;60&amp;#37; of the 180 BHAV bioindicator (157 plant, 4 ixodid tick, and 19 vertebrate spp.). On that basis, Greece, France (southern, including Corsica), Albania, Spain, Hungary, European Turkey, Ukraine (southern), Switzerland (southern), Austria (southeastern), Germany (southern), Moldova, and European Russia (southern) have been predicted as additional European regions where BHAV might occur.</description><Author>Zdenek Hub&amp;#225;lek</Author><copyright>&amp;#169; 2010, Hindawi Publishing Corporation. All rights reserved.</copyright></item><item><title>Towards an Understanding of the Herpes Simplex Virus Type 1 Latency-Reactivation Cycle</title><link>http://www.hindawi.com/journals/ipid/2010/262415.html</link><description>Infection by herpes simplex virus type 1 (HSV-1) can cause clinical symptoms in the peripheral and central nervous system. Recurrent ocular shedding can lead to corneal scarring and vision loss making HSV-1 a leading cause of corneal blindness due to an infectious agent. The primary site of HSV-1 latency is sensory neurons within trigeminal ganglia. Periodically, reactivation from latency occurs resulting in virus transmission and recurrent disease. During latency, the latency-associated transcript (LAT) is abundantly expressed. LAT expression is important for the latency-reactivation cycle in animal models, in part, because it inhibits apoptosis, viral gene expression, and productive infection. A novel transcript within LAT coding sequences (AL3) and small nonprotein coding RNAs are also expressed in trigeminal ganglia of latently infected mice. In this review, an update of viral factors that are expressed during latency and their potential roles in regulating the latency-reactivation cycle is discussed.</description><Author>Guey-Chuen Perng and Clinton Jones</Author><copyright>&amp;#169; 2010, Hindawi Publishing Corporation. All rights reserved.</copyright></item><item><title>Immunogenetics and the Pathological Mechanisms of Human T-Cell Leukemia Virus Type 1- (HTLV-1-)Associated Myelopathy/Tropical Spastic Paraparesis (HAM/TSP)</title><link>http://www.hindawi.com/journals/ipid/2010/478461.html</link><description>Human T-cell leukemia virus type 1 (HTLV-1) is a replication-competent human retrovirus associated with two distinct types of disease only in a minority of infected individuals: the malignancy known as adult T-cell leukemia (ATL) and a chronic inflammatory central nervous system disease HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP). Although the factors that cause these different manifestations of HTLV-1 infection are not fully understood, accumulating evidence suggests that complex virus-host interactions play an important role in determining the risk of HAM/TSP. This review focuses on the role of the immune response in controlling or limiting viral persistence in HAM/TSP patients, and the reason why some HTLV-1-infected people develop HAM/TSP whereas the majority remains asymptomatic carriers of the virus.</description><Author>Mineki Saito</Author><copyright>&amp;#169; 2010, Hindawi Publishing Corporation. All rights reserved.</copyright></item><item><title>Parasitic Diseases, Diagnostic Approaches, and Therapies</title><link>http://www.hindawi.com/journals/ipid/2009/893890.html</link><description /><Author>Herbert B. Tanowitz and Louis M. Weiss</Author><copyright>&amp;#169; 2010, Hindawi Publishing Corporation. All rights reserved.</copyright></item><item><title>COMT Val158Met Polymorphism, Executive Dysfunction, and Sexual Risk Behavior in the Context of HIV Infection and Methamphetamine Dependence</title><link>http://www.hindawi.com/journals/ipid/2010/678648.html</link><description>Catechol-O-methyltransferease (COMT) metabolizes prefrontal cortex dopamine (DA), a neurotransmitter involved in executive behavior; the Val158Met genotype has been linked to executive dysfunction, which might increase sexual risk behaviors favoring HIV transmission. Main and interaction effects of COMT genotype and executive functioning on sexual risk behavior were examined. 192 sexually active nonmonogamous men completed a sexual behavior questionnaire, executive functioning tests, and were genotyped using blood-derived DNA. Main effects for executive dysfunction but not COMT on number of sexual partners were observed. A COMT x executive dysfunction interaction was found for number of sexual partners and insertive anal sex, significant for carriers of the Met/Met and to a lesser extent Val/Met genotypes but not Val/Val carriers. In the context of HIV and methamphetamine dependence, dopaminergic overactivity in prefrontal cortex conferred by the Met/Met genotype appears to result in a liability for executive dysfunction and potentially associated risky sexual behavior.</description><Author>C. A. Bousman, M. Cherner, J. H. Atkinson, R. K. Heaton, I. Grant, I. P. Everall, and The HNRC Group</Author><copyright>&amp;#169; 2010, Hindawi Publishing Corporation. All rights reserved.</copyright></item><item><title>Diagnosis of Parasitic Diseases: Old and New Approaches</title><link>http://www.hindawi.com/journals/ipid/2009/278246.html</link><description>Methods for the diagnosis of infectious diseases have stagnated in the last 20&amp;#8211;30 years. Few major advances in clinical diagnostic testing have been made since the introduction of PCR, although new technologies are being investigated. Many tests that form the backbone of the &amp;#8220;modern&amp;#8221; microbiology laboratory are based on very old and labour-intensive technologies such as microscopy for malaria. Pressing needs include more rapid tests without sacrificing sensitivity, value-added tests, and point-of-care tests for both high- and low-resource settings. In recent years, research has been focused on alternative methods to improve the diagnosis of parasitic diseases. These include immunoassays, molecular-based approaches, and proteomics using mass spectrometry platforms technology. This review summarizes the progress in new approaches in parasite diagnosis and discusses some of the merits and disadvantages of these tests.</description><Author>Momar Ndao</Author><copyright>&amp;#169; 2010, Hindawi Publishing Corporation. All rights reserved.</copyright></item><item><title>Procalcitonin as a Biomarker for a Bacterial Infection on Hospital Admission: A Critical Appraisal in a Cohort of Travellers with Fever after a Stay in (Sub)tropics</title><link>http://www.hindawi.com/journals/ipid/2009/137609.html</link><description>Fever in a returned traveller may be the manifestation of a self-limiting, trivial infection but it can also presage an infection that can be rapidly progressive and lethal. We studied the diagnostic accuracy of procalcitonin (PCT) as a biomarker for a bacterial cause of fever in a cohort of 157 consecutive travellers with fever after a stay in the (sub)tropics. Elevated procalcitonin levels were observed not only in about 50&amp;#37; of travellers with proven bacterial infection, but also in a significant proportion of travellers with a likely infection. Using a cutoff point of 0.5&amp;#x2009;ng/mL, procalcitonin had a sensitivity of 0.52 and a specificity of 0.76 for a bacterial cause of fever on admission. Interestingly, only 1 out of 16 patients with a proven viral infection had a marginally elevated PCT concentration on admission, suggesting that an increased PCT level likely excludes a viral infection as the cause of fever. However, the diagnostic accuracy of this semiquantitative procalcitonin test for a bacterial cause of fever on admission is too poor to advocate its use in the initial clinical evaluation of fever in a setting of ill-returned travellers.</description><Author>Dennis A. Hesselink, Hanna Bosmans-Timmerarends, Jan-Steven Burgerhart, Pieter L. Petit, and Perry J. van Genderen</Author><copyright>&amp;#169; 2010, Hindawi Publishing Corporation. All rights reserved.</copyright></item><item><title>In Vitro Synergy of Levofloxacin Plus Piperacillin/Tazobactam against Pseudomonas aeruginosa</title><link>http://www.hindawi.com/journals/ipid/2009/984934.html</link><description>In vitro synergy testing using levofloxacin (LVX) plus piperacillin/tazobactam (TZP) was performed by Etest and time-kill assay (TKA) for 31 unique fluoroquinolone-resistant Pseudomonas aeruginosa isolates. The Etest method showed synergy for 9/31 (29&amp;#37;) of isolates, while TKA showed synergy with 14/31 (45&amp;#37;) of isolates. When comparing the Etest method and TKA, concordant results for synergy, antagonism, and indifference were obtained for 24/31 (77&amp;#37;) of the isolates tested.</description><Author>Vladimir Chachanidze, Aixa Curbelo-Irizarry, Deborah Ashcraft, and George Pankey</Author><copyright>&amp;#169; 2010, Hindawi Publishing Corporation. All rights reserved.</copyright></item><item><title>Human Cystic Echinococcosis: Old Problems and New Perspectives</title><link>http://www.hindawi.com/journals/ipid/2009/474368.html</link><description>Cystic echinococcosis (CE) is a widespread chronic endemic helminthic disease caused by infection with metacestodes of the tapeworm Echinococcus granulosus. CE affects humans and has a worldwide prevalence of approximately six million. In this review, we discuss current findings in diagnosis and clinical management of CE and new concepts relating to E. granulosus molecules that directly modulate the host immune responses favouring a strong anti-inflammatory response and perpetuating parasite survival in the host. New insights into the molecular biology of E. granulosus will improve considerably our knowledge of the disease and will provide new potential therapeutic applications to treat or prevent inflammatory immune-mediated disease.</description><Author>Alessandra Siracusano, Antonella Teggi, and Elena Ortona</Author><copyright>&amp;#169; 2010, Hindawi Publishing Corporation. All rights reserved.</copyright></item><item><title>B Cell IgD Deletion Prevents Alveolar Bone Loss Following Murine Oral Infection</title><link>http://www.hindawi.com/journals/ipid/2009/864359.html</link><description>Periodontal disease is one of the most common infectious diseases of humans. Immune
responses to infection trigger loss of alveolar bone from the jaw and eventual tooth loss. We investigated the contribution of B cell IgD to alveolar bone loss by comparing the response of B cell normal BALB/cJ mice and IgD deficient BALB/c-Igh-5&amp;#x02212;/&amp;#x02212;J mice to oral infection with Porphyromonas gingivalis, a gram-negative periodontopathic bacterium
from humans. P. gingivalis-infected normal mice lost bone. Specific antibody to P. gingivalis was lower and oral colonization was higher in IgD deficient mice; yet bone loss was completely absent. Infection increased the proportion of CD69+ activated B cells
and CD4+ T cells in immune normal mice compared to IgD deficient mice. These data suggest that IgD is an important mediator of alveolar bone resorption, possibly through antigen-specific coactivation of B cells and CD4+ T cells.</description><Author>Pamela J. Baker, Nicole Ryan Boutaugh, Michaela Tiffany, and Derry C. Roopenian</Author><copyright>&amp;#169; 2010, Hindawi Publishing Corporation. All rights reserved.</copyright></item><item><title>Antibiotic-Resistant Gram Negative Bacilli in Meals Delivered at a General Hospital, Italy</title><link>http://www.hindawi.com/journals/ipid/2009/476150.html</link><description>This study aimed at detecting the presence of antibiotic-resistant Gram-negatives in samples of meals delivered at the University General Hospital of  Palermo, Italy. Antibiotic resistant Gram negatives were isolated in July&amp;#x02014;September 2007 ffrom cold dishes and food contact surfaces and utensils. Bacterial strains were submitted to susceptibility test and subtyped by random amplification of polymorphic DNA (RAPD).  Forty-six of 55 (83.6&amp;#37;) food samples and 14 of 17 (82.3&amp;#37;) environmental swabs were culture positive for Gram negative bacilli resistant to at least one group of antibacterial drugs. A total of 134 antibiotic resistant strains, 51 fermenters and 83 non-fermenters, were recovered. Fermenters and non-fermenters showed frequencies as high as 97.8&amp;#37; of resistance to two or more groups of antibiotics and non fermenters were 28.9&amp;#37; resistant to more than three groups. Molecular typing detected 34 different profiles among the fermenters and 68 among the non-fermenters. Antibiotic resistance was very common among both fermenters and non-fermenters. However, the wide heterogeneity of RAPD patterns seems to support a prominent role of cross-contamination rather than a clonal expansion of a few resistant isolates. A contribution of commensal Gram negatives colonizing foods to a common bacterial resistance pool should not been overlooked.</description><Author>Maria Rosa Anna Plano, Anna Maria Di Noto, Alberto Firenze, Sonia Sciortino, and Caterina Mammina</Author><copyright>&amp;#169; 2010, Hindawi Publishing Corporation. All rights reserved.</copyright></item><item><title>Diagnosis and Treatment of Neurocysticercosis</title><link>http://www.hindawi.com/journals/ipid/2009/180742.html</link><description>Neurocysticercosis, the infection caused by the larval form of the tapeworm Taenia solium, is the most common parasitic disease of the central nervous system and the most common cause of acquired epilepsy worldwide. This has primarily been a disease that remains endemic in low-socioeconomic  countries, but because of increased migration neurocysticercosis is being diagnosed more frequently in high-income countries. During the past three decades improved diagnostics, imaging, and treatment have led to more accurate diagnosis and improved prognosis for patients. This article reviews the current literature on neurocysticercosis, including newer diagnostics and treatment developments.</description><Author>Christina M. Coyle and Herbert B. Tanowitz</Author><copyright>&amp;#169; 2010, Hindawi Publishing Corporation. All rights reserved.</copyright></item><item><title>Update on Babesiosis</title><link>http://www.hindawi.com/journals/ipid/2009/984568.html</link><description>Human babesiosis is an emerging tick-borne infectious disease caused by intraerythrocytic protozoan species of the genus Babesia with many clinical features similar to those of malaria. Over the last 50 years, the epidemiology of human babesiosis has changed from a few isolated cases to the establishment of endemic areas in the northeastern and midwestern United States. Episodic cases are reported in Europe, Asia, Africa, and South America. The severity of infection ranges from asymptomatic infection to fulminant disease resulting in death, although the majority of healthy adults experience a mild-to-moderate illness. People over the age of 50 years and immunocompromised individuals are at the highest risk of severe disease, including those with malignancy, HIV, lacking a spleen, or receiving immunosuppressive drugs. Asymptomatic carriers present a blood safety risk when they donate blood. Definitive diagnosis of babesial infection generally is made by microscopic identification of the organism on thin blood smear, amplification of Babesia DNA using PCR, and detection of Babesia antibody in acute and convalescent sera. Specific antimicrobial therapy consists of atovaquone and azithromycin or clindamycin and quinine. Exchange transfusion is used in severe cases. The use of multiple prevention strategies is recommended and consists of personal, residential, and community approaches.</description><Author>Edouard Vannier and Peter J. Krause</Author><copyright>&amp;#169; 2010, Hindawi Publishing Corporation. All rights reserved.</copyright></item><item><title>Chemotherapy of  Human  African Trypanosomiasis</title><link>http://www.hindawi.com/journals/ipid/2009/195040.html</link><description>Human Africa trypanosomiasis is a centuries-old disease which has disrupted sub-Saharan Africa in both physical suffering and economic loss. This article presents an update of classic chemotherapeutic agents, in use for &amp;gt;50 years and the recent development of promising non-toxic combination chemotherapy suitable for use in rural clinics.</description><Author>Cyrus J. Bacchi</Author><copyright>&amp;#169; 2010, Hindawi Publishing Corporation. All rights reserved.</copyright></item><item><title>The Impact of HIV and Malaria Coinfection: What Is Known and Suggested Venues for Further Study</title><link>http://www.hindawi.com/journals/ipid/2009/617954.html</link><description>HIV and malaria have similar global distributions. Annually, 500 million are infected and 1 million die because of malaria. 33 million have HIV and 2 million die from it each year. Minor effects of one infection on the disease course or outcome for the other would significantly impact public health because of the sheer number of people at risk for coinfection. While early population-based studies showed no difference in outcomes between HIV-positive and HIV-negative individuals with malaria, more recent work suggests that those with HIV have more frequent episodes of symptomatic malaria and that malaria increases HIV plasma viral load and decreases CD4+ T cells. HIV and malaria each interact with the host&amp;#39;s immune system, resulting in a complex activation of immune cells, and subsequent dysregulated production of cytokines and antibodies. Further investigation of these interactions is needed to better define effects of coinfection.</description><Author>Sarah Hochman and Kami Kim</Author><copyright>&amp;#169; 2010, Hindawi Publishing Corporation. All rights reserved.</copyright></item><item><title>Sterol Biosynthesis Pathway as Target for Anti-trypanosomatid Drugs</title><link>http://www.hindawi.com/journals/ipid/2009/642502.html</link><description>Sterols are constituents of the cellular membranes that are essential for their normal structure and function. In mammalian cells, cholesterol is the main sterol found in the various membranes. However, other sterols predominate in eukaryotic microorganisms such as fungi and protozoa. It is now well established that an important metabolic pathway in fungi and in members of the Trypanosomatidae family is one that produces a special class of sterols, including ergosterol, and other 24-methyl sterols, which are required for parasitic growth and viability, but are absent from mammalian host cells. Currently, there are several drugs that interfere with sterol biosynthesis (SB) that are in use to treat diseases such as high cholesterol in humans and fungal infections. In this review, we analyze the effects of drugs such as (a) statins, which act on the mevalonate pathway by inhibiting HMG-CoA reductase, (b) bisphosphonates, which interfere with the isoprenoid pathway in the step catalyzed by farnesyl diphosphate synthase, (c) zaragozic acids and quinuclidines, inhibitors of squalene synthase (SQS), which catalyzes the first committed step in sterol biosynthesis, (d) allylamines, inhibitors of squalene epoxidase, (e) azoles, which inhibit C14&amp;#x03B1;-demethylase, and (f) azasterols, which inhibit &amp;#x0394;24(25)-sterol methyltransferase (SMT). Inhibition of this last step appears to have high selectivity for fungi and trypanosomatids, since this enzyme is not found in mammalian cells. We review here the IC50 values of these various inhibitors, their effects on the growth of trypanosomatids (both in axenic cultures and in cell cultures), and their effects on protozoan structural organization (as evaluted by light and electron microscopy) and lipid composition. The results show that the mitochondrial membrane as well as the membrane lining the protozoan cell body and flagellum are the main targets. Probably as a consequence of these primary effects, other important changes take place in the organization of the kinetoplast DNA network and on the protozoan cell cycle. In addition, apoptosis-like and autophagic processes induced by several of the inhibitors tested led to parasite death.</description><Author>Wanderley de Souza and Juliany Cola Fernandes Rodrigues</Author><copyright>&amp;#169; 2010, Hindawi Publishing Corporation. All rights reserved.</copyright></item><item><title>Diagnosis of Infections Caused by Pathogenic Free-Living Amoebae</title><link>http://www.hindawi.com/journals/ipid/2009/251406.html</link><description>Naegleria fowleri, Acanthamoeba spp., Balamuthia mandrillaris, and Sappinia sp. are pathogenic free-living amoebae. N. fowleri causes Primary Amoebic Meningoencephalitis, a rapidly fatal disease of the central nervous system, while Acanthamoeba spp. and B. mandrillaris cause chronic granulomatous encephalitis. Acanthamoeba spp. also can cause cutaneous lesions and Amoebic Keratitis, a sight-threatening infection of the cornea that is associated with contact lens use or corneal trauma. Sappinia pedata has been identified as the cause of a nonlethal case of amoebic encephalitis. In view of the potential health consequences due to infection with these amoebae, rapid diagnosis is critical for early treatment. Microscopic examination and culture of biopsy specimens, cerebral spinal fluid (CSF), and corneal scrapings have been used in the clinical laboratory. For amoebic keratitis, confocal microscopy has been used to successfully identify amoebae in corneal tissue. More recently, conventional and real-time PCR assays have been developed that are sensitive and specific for the amoebae. In addition, multiplex PCR assays are available for the rapid identification of these pathogens in biopsy tissue, CSF, and corneal specimens.</description><Author>Bruno da Rocha-Azevedo, Herbert B. Tanowitz, and Francine Marciano-Cabral</Author><copyright>&amp;#169; 2010, Hindawi Publishing Corporation. All rights reserved.</copyright></item><item><title>Molecular Diagnostic Tests for Microsporidia</title><link>http://www.hindawi.com/journals/ipid/2009/926521.html</link><description>The Microsporidia are a ubiquitous group of eukaryotic obligate intracellular parasites which were recognized over 100 years ago with the description of Nosema bombycis, a parasite of silkworms. It is now appreciated that these organisms are related to the Fungi. Microsporidia infect all major animal groups most often as gastrointestinal pathogens; however they have been reported from every tissue and organ, and their spores are common in environmental sources such as ditch water. Several different genera of these organisms infect humans, but the majority of infections are due to either 
Enterocytozoon bieneusi or Encephalitozoon species. These pathogens can be difficult to diagnose, but significant progress has been made in the last decade in the development of molecular diagnostic reagents for these organisms. This report reviews the molecular diagnostic tests that have been described for the identification of the microsporidia that infect humans.</description><Author>Kaya Ghosh and Louis M. Weiss</Author><copyright>&amp;#169; 2010, Hindawi Publishing Corporation. All rights reserved.</copyright></item><item><title>Perspectives on Adipose Tissue, Chagas Disease and Implications for the Metabolic Syndrome</title><link>http://www.hindawi.com/journals/ipid/2009/824324.html</link><description>The contribution of adipose tissue an 
                  autocrine and endocrine organ in the 
                  pathogenesis of infectious disease and metabolic 
                  syndrome is gaining attention. Adipose tissue 
                  and adipocytes 
are one of the major targets of T. cruzi infection. Parasites are detected 300 days postinfection in adipose tissue. Infection of adipose tissue and cultured adipocytes triggered local
expression of inflammatory mediators resulting in the upregulation of cytokine and chemokine
levels. Adipose tissue obtained from infected mice display an increased infiltration of
inflammatory cells. Adiponectin, an adipocyte specific protein, which exerts antiinflammatory
effects, is reduced during the acute phase of infection. The antiinflammatory regulator
peroxisome proliferator activated receptor-&amp;#x03B3; (PPAR-&amp;#x03B3;) is downregulated in infected cultured
adipocytes and adipose tissue. T. cruzi infection is associated with an upregulation of signaling
pathways such as MAPKs, Notch and cyclin D, and reduced caveolin-1 expression.
Adiponectin null mice have a cardiomyopathy and thus we speculate that the T. cruzi-induced
reduction in adiponectin contributes to the T. cruzi-induced cardiomyopathy. While T. cruzi infection causes hypoglycemia which correlates with mortality, hyperglycemia is associated
with increased parasitemia and mortality. The T. cruzi-induced increase in macrophages in
adipose tissue taken together with the reduction in adiponectin and the associated
cardiomyopathy is reminiscent of the metabolic syndrome.</description><Author>Fnu Nagajyothi, Mahalia S. Desruisseaux, Linda A. Jelicks, Fabiana S. Machado, Streamson Chua, Philipp E. Scherer, and Herbert B. Tanowitz</Author><copyright>&amp;#169; 2010, Hindawi Publishing Corporation. All rights reserved.</copyright></item><item><title>Rapid Diagnosis of Intestinal Parasitic Protozoa, with a Focus on Entamoeba histolytica</title><link>http://www.hindawi.com/journals/ipid/2009/547090.html</link><description>Entamoeba histolytica is an invasive intestinal pathogenic parasitic protozoan that causes amebiasis. It must be distinguished from Entamoeba dispar and E. moshkovskii, nonpathogenic commensal parasites of the human gut lumen that are morphologically identical to E. histolytica. Detection of specific E. histolytica antigens in stools is a fast, sensitive technique that should be considered as the method of choice. Stool real-time PCR is a highly sensitive and specific technique but its high cost make it unsuitable for use in endemic areas where there are economic constraints. Serology is an important component of the diagnosis of intestinal and especially extraintestinal amebiasis as it is a sensitive test that complements the detection of the parasite antigens or DNA. Circulating Gal/GalNac lectin antigens can be detected in the serum of patients with untreated amoebic liver abscess. On the horizon are multiplex real-time PCR assays which permit the identification of multiple enteropathogens with high sensitivity and specificity.</description><Author>Anjana Singh, Eric Houpt, and William A. Petri</Author><copyright>&amp;#169; 2010, Hindawi Publishing Corporation. All rights reserved.</copyright></item><item><title>Oxidative Stress in Chagas Disease</title><link>http://www.hindawi.com/journals/ipid/2009/190354.html</link><description>There is growing evidence to suggest that chagasic myocardia are exposed to sustained oxidative stress induced injuries that may contribute to disease progression. Trypanosoma cruzi invasion- and replication-mediated cellular injuries and immune-mediated cytotoxic reactions are the common source of reactive oxygen species (ROS) during acute infection. Mitochondria are proposed to be the major source of ROS in chronic chagasic hearts. However, it has not been established yet, whether mitochondrial dysfunction is a causative factor in chagasic cardiomyopathy or a consequence of other pathological events. A better understanding of oxidative stress in relation to cardiac tissue damage would be useful in the evaluation of its true role in the pathogenesis of Chagas disease and other heart diseases. In this review, we discuss the evidence for increased oxidative stress in chagasic disease, with emphasis on mitochondrial abnormalities, and its role in sustaining oxidative stress in myocardium.</description><Author>Shivali Gupta, Jian-Jun Wen, and Nisha Jain Garg</Author><copyright>&amp;#169; 2010, Hindawi Publishing Corporation. All rights reserved.</copyright></item><item><title>Over the Counter Availability of Antituberculosis Drugs in Tbilisi, Georgia in the Setting of a High Prevalence of MDR-TB</title><link>http://www.hindawi.com/journals/ipid/2009/513609.html</link><description>Georgia, a country of 4.5 million people, has a high incidence of tuberculosis (TB) including drug resistant cases. Easy access and inappropriate use of anti-TB drugs are risk factors for further development of multidrug resistant (MDR)-TB. We carried out an investigation to assess the availability of over the counter anti-TB agents in pharmacies in Tbilisi. During February 2006, 15 pharmacies were randomly selected and the pharmacist at each store was interviewed. We found that all anti-TB medications stocked by these pharmacies were available and sold without a prescription. All 15 pharmacies sold isoniazid, rifampicin, and streptomycin; 13 (87&amp;#x25;) of 15 pharmacies also sold pyrazinamide, ethambutol. Second line anti-TB drugs such as amikacin and kanamycin (injectable agents) and older fluoroquinolones (ofloxacin and ciprofloxacin) were available at 13 pharmacies while newer generation fluoroquinolones were less available(3 sold leovofloxacin, none sold moxifloxacin). The ease access and availability of anti-TB agents is of a great concern given the high prevalence of TB including MDR-TB in Georgia. The potential for misuse of these anti-TB drugs can lead to the development of further drug resistance. These drugs should only be available by prescription in order to
reduce the chance of amplifying drug resistance.</description><Author>Ketevan Kobaidze, Archil Salakaia, and Henry M. Blumberg</Author><copyright>&amp;#169; 2010, Hindawi Publishing Corporation. All rights reserved.</copyright></item><item><title>Cell Therapy in Chagas Disease</title><link>http://www.hindawi.com/journals/ipid/2009/484358.html</link><description>Chagas disease which is caused by the parasite Trypanosoma cruzi is an important cause of cardiomyopathy in Latin America. In later stages chagasic cardiomyopathy is associated with congestive heart failure which is often refractory to medical therapy. In these individuals heart transplantation has been attempted. However, this procedure is fraught with many problems attributable to the surgery and the postsurgical administration of immunosuppressive drugs. Studies in mice suggest that the transplantation of bone-marrow-derived cells ameliorates the inflammation and fibrosis in the heart associated with this infection. Cardiac magnetic resonance imaging reveals that bone marrow transplantation ameliorates the infection induced right ventricular enlargement. On the basis of these animal studies the safety of autologous bone marrow transplantation has been assessed in patients with chagasic end-stage heart disease. The initial results are encouraging and more studies need to be performed.</description><Author>Antonio C. Campos de Carvalho, Regina C. S. Goldenberg, Linda A. Jelicks, Milena B. P. Soares, Ricardo Ribeiro dos Santos, David C. Spray, and Herbert B. Tanowitz</Author><copyright>&amp;#169; 2010, Hindawi Publishing Corporation. All rights reserved.</copyright></item><item><title>Rapid Diagnosis of Malaria</title><link>http://www.hindawi.com/journals/ipid/2009/415953.html</link><description>Malaria&amp;#39;s global impact is expansive and includes the extremes of the healthcare system ranging from international travelers returning to nonendemic regions with tertiary referral medical care to residents in hyperendemic regions without access to medical care. Implementation of prompt and accurate diagnosis is needed to curb the expanding global impact of malaria associated with ever-increasing antimalarial drug resistance. Traditionally, malaria is diagnosed using clinical criteria and/or light microscopy even though both strategies are clearly inadequate in many healthcare settings. Hand held immunochromatographic rapid diagnostic tests (RDTs) have been recognized as an ideal alternative method for diagnosing malaria. Numerous malaria RDTs have been developed and are widely available; however, an assortment of issues related to these products have become apparent. This review provides a summary of RDT including effectiveness and strategies to select the ideal RDT in varying healthcare settings.</description><Author>Clinton K. Murray and Jason W. Bennett</Author><copyright>&amp;#169; 2010, Hindawi Publishing Corporation. All rights reserved.</copyright></item><item><title>New Means of Canine Leishmaniasis Transmission in North America: The Possibility of Transmission to Humans Still Unknown</title><link>http://www.hindawi.com/journals/ipid/2009/802712.html</link><description>At present it is not possible to determine in advance the outcome of Leishmania infantum infection. Canine Visceral Leishmaniasis (VL), caused by Le. infantum, is a natural disease process which offers a insight into the interaction of the host and resultant disease outcome. Canine VL results in the same altered pathophysiology and immunodysregulation seen in humans. VL in US dogs is likely to be transmitted primarily via nontraditional, nonvector means. VL mediated by Le. infantum is endemic in U.S. Foxhound dogs, with vertical transmission likely to be the novel primary means of transmission. This population of dogs offers an opportunity to identify host factors of natural disease. Prevention of human clinical visceral leishmaniasis can occur only by better understanding the disease ecology of the primary reservoir host: the dog.</description><Author>Christine A. Petersen</Author><copyright>&amp;#169; 2010, Hindawi Publishing Corporation. All rights reserved.</copyright></item><item><title>Could Proteomic Research Deliver the Next Generation of Treatments for Pneumococcal Meningitis?</title><link>http://www.hindawi.com/journals/ipid/2009/214216.html</link><description>Streptococcus pneumoniae is the most common bacterial cause of community-acquired meningitis worldwide. Despite optimal antibiotic therapy and supportive care, the mortality of this condition remains very high at 20&amp;#8211;30&amp;#37; in the developed world and over 60&amp;#37; in under-resourced hospitals. In developed countries, approximately half of the survivors suffer intellectual impairment, hearing loss, or other neurological damage. There is an urgent need for more information about the mechanisms of brain damage and death in pneumococcal meningitis so that new treatments can be designed. Using proteomic techniques and bioinformatics, the protein content of cerebrospinal fluid can be examined in great detail. Animal models have added greatly to our knowledge of possible mechanisms and shown that hippocampal apoptosis and cortical necrosis are distinct mechanisms of neuronal death. The contribution of these pathways to human disease is unknown. Using proteomic techniques, neuronal death pathways could be described in CSF samples. This information could lead to the design of novel therapies to minimize brain damage and lower mortality. This minireview will summarize the known pathogenesis of meningitis, and current gaps in knowledge, that could be filled by proteomic analysis.</description><Author>U. R. Goonetilleke, S. A. Ward, and S. B. Gordon</Author><copyright>&amp;#169; 2010, Hindawi Publishing Corporation. All rights reserved.</copyright></item></channel></rss>