Scabies masquerading as Letterer-Siwe's disease.

Letterer-Siwe''s disease was diagnosed from clinical appearance and initial assessment of a skin biopsy in a child with a 2-month history of skin rash. Fine erythematous papules were scattered on the trunk. The biopsy showed epidermal thickening and an inflammatory infiltrate chiefly in the upper layers of the dermis; deeper in the dermis the infiltrate was perivascular and periappendicular, histiocytes predominating in some areas and lymphocytes in others. A diagnosis of scabies was made after burrows were demonstrated on palms and soles and the mite of scabies was isolated from them.     

Bartonella interactions with endothelial cells and erythrocytes

Bartonella species are emerging human pathogens responsible for a wide range of clinical manifestations, including Carrion's disease, trench fever, cat-scratch disease, bacillary angiomatosis-peliosis, endocarditis and bacteraemia. During infection of their human or animal reservoir host(s), these arthropod-borne pathogens typically invade and persistently colonize mature erythrocytes. However, in both reservoir and incidentally infected hosts, endothelial cells are target cells for bartonellae. Endothelial interactions involve a unique mode of cellular invasion, the activation of a proinflammatory phenotype and the formation of vasoproliferative tumours. Based on the establishment of bacterial genetics and appropriate infection models, recent work has begun to elucidate the cell and molecular biology of these unusual pathogen-host cell interactions.     

Prediction of host-pathogen protein interactions by extended network model

Knowledge of the pathogen-host interactions between the species is essentialin order to develop a solution strategy against infectious diseases. In vitro methods take extended periods of time to detect interactions and provide very few of the possible interaction pairs. Hence, modelling interactions between proteins has necessitated the development of computational methods. The main scope of this paper is integrating the known protein interactions between thehost and pathogen organisms to improve the prediction success rate of unknown pathogen-host interactions. Thus, the truepositive rate of the predictions was expected to increase.In order to perform this study extensively, encoding methods and learning algorithms of several proteins were tested. Along with human as the host organism, two different pathogen organisms were used in the experiments. For each combination of protein-encoding and prediction method, both the original prediction algorithms were tested using only pathogen-host interactions and the same methodwas testedagain after integrating the known protein interactions within each organism. The effect of merging the networks of pathogen-host interactions of different species on the prediction performance of state-of-the-art methods was also observed. Successwas measured in terms of Matthews correlation coefficient, precision, recall, F1 score, and accuracy metrics. Empirical results showed that integrating the host and pathogen interactions yields better performance consistently in almost all experiments.     

Host-induced gene silencing: a tool for understanding fungal host interaction and for developing novel disease control strategies

Recent discoveries regarding small RNAs and the mechanisms of gene silencing are providing new opportunities to explore fungal pathogen-host interactions and potential strategies for novel disease control. Plant pathogenic fungi are a constant and major threat to global food security; they represent the largest group of disease-causing agents on crop plants on the planet. An initial understanding of RNA silencing mechanisms and small RNAs was derived from model fungi. Now, new knowledge with practical implications for RNA silencing is beginning to emerge from the study of plant-fungus interactions. Recent studies have shown that the expression of silencing constructs in plants designed on fungal genes can specifically silence their targets in invading pathogenic fungi, such as Fusarium verticillioides, Blumeria graminis and Puccinia striiformis f.sp. tritici. Here, we highlight the important general aspects of RNA silencing mechanisms and emphasize recent findings from plant pathogenic fungi. Strategies to employ RNA silencing to investigate the basis of fungal pathogenesis are discussed. Finally, we address important aspects for the development of fungal-derived resistance through the expression of silencing constructs in host plants as a powerful strategy to control fungal disease.     

The pathogen-host interactions database (PHI-base) provides insights into generic and novel themes of pathogenicity

Fungal and oomycete pathogens of plants and animals are a major global problem. In the last 15 years, many genes required for pathogenesis have been determined for over 50 different species. Other studies have characterized effector genes (previously termed avirulence genes) required to activate host responses. By studying these types of pathogen genes, novel targets for control can be revealed. In this report, we describe the Pathogen-Host Interactions database (PHI-base), which systematically compiles such pathogenicity genes involved in pathogen-host interactions. Here, we focus on the biology that underlies this computational resource: the nature of pathogen-host interactions, the experimental methods that exist for the characterization of such pathogen-host interactions as well as the available computational resources. Based on the data, we review and analyze the specific functions of pathogenicity genes, the host-specific nature of pathogenicity and virulence genes, and the generic mechanisms of effectors that trigger plant responses. We further discuss the utilization of PHI-base for the computational identification of pathogenicity genes through comparative genomics. In this context, the importance of standardizing pathogenicity assays as well as integrating databases to aid comparative genomics is discussed.     

Latency of Baculoviruses

Due to their widespread natural occurrence, baculoviruses and their insect hosts are a convenient model to study the pathogen-host interactions. However, the absence of reliable techniques for the detection of latent viral infection, which is common in insect populations, is among the constraints of such studies. The recent progress in molecular biology techniques made it possible to obtain the fundamental data on the detection of latent viruses in different insect species as well as on the mechanism of latent infection induction, which are reviewed below. The obtained data in many respects expand our knowledge about the role of latency in the system of interactions between baculoviruses and their insect hosts at different ecological levels.     

Parasite-host glycan interactions during Trypanosoma cruzi infection: trans-Sialidase rides the show

Many important pathogen-host interactions rely on highly specific carbohydrate binding events. In the case of the protozoan Trypanosoma cruzi, the causative agent of Chagas disease, glycointeractions involving sialic acid (SA) residues are pivotal for parasite infectivity, escape from immune surveillance and pathogenesis. Though unable to synthesize SA de novo, T. cruzi displays a unique trans-Sialidase (TS) enzyme, which is able to cleave terminal SA residues from host donor glycoconjugates and transfer them onto parasite surface mucins, thus generating protective/adhesive structures. In addition, this parasite sheds TS into the bloodstream, as a way of modifying the surface SA signature, and thereby the signaling/functional properties of mammalian host target cells on its own advantage. Here, we discuss the pathogenic aspects of T. cruzi TS: its molecular adaptations, the multiplicity of interactions in which it is involved during infections, and the array of novel and appealing targets for intervention in Chagas disease provided by TS-remodeled sialoglycophenotypes.     

Ecology of invasive mosquitoes: effects on resident species and on human health

Investigations of biological invasions focus on patterns and processes that are related to introduction, establishment, spread and impacts of introduced species. This review focuses on the ecological interactions operating during invasions by the most prominent group of insect vectors of disease, mosquitoes. First, we review characteristics of non-native mosquito species that have established viable populations, and those invasive species that have spread widely and had major impacts, testing whether biotic characteristics are associated with the transition from established non-native to invasive. Second, we review the roles of interspecific competition, apparent competition, predation, intraguild predation and climatic limitation as causes of impacts on residents or as barriers to invasion. We concentrate on the best-studied invasive mosquito, Aedes albopictus, evaluating the application of basic ecological theory to invasions by Aedes albopictus. We develop a model based on observations of Aedes albopictus for effects of resource competition and predation as barriers to invasion, evaluating which community and ecosystem characteristics favour invasion. Third, we evaluate the ways in which invasive mosquitoes have contributed to outbreaks of human and animal disease, considering specifically whether invasive mosquitoes create novel health threats, or modify disease transmission for existing pathogen-host systems.     

Systems biology of pathogen-host interaction: Networks of protein-protein interaction within pathogens and pathogen-human interactions in the post-genomic era

Infectious diseases comprise some of the leading causes of death and disability worldwide. Interactions between pathogen and host proteins underlie the process of infection. Improved understanding of pathogen-host molecular interactions will increase our knowledge of the mechanisms involved in infection, and allow novel therapeutic solutions to be devised. Complete genome sequences for a number of pathogenic microorganisms, as well as the human host, has led to the revelation of their protein-protein interaction (PPI) networks. In this post-genomic era, pathogen-host interactions (PHIs) operating during infection can also be mapped. Detailed systematic analyses of PPI and PHI data together are required for a complete understanding of pathogenesis of infections. Here we review the striking results recently obtained during the construction and investigation of these networks. Emphasis is placed on studies producing large-scale interaction data by high-throughput experimental techniques.     

Organoids in recapitulating tumorigenesis driven by risk factors: Current trends and future perspectives

Environmental and exogenous/ endogenous factors, in a setting of individual genetic predisposition, contribute to the cancer development. Over the years, epidemical evidence increasingly highlights the correlations of multiple cancer incentives and genetic alterations with cancer incidence. Unraveling the pivotal carcinogenesis events prompted by particular risk factors remarkably advances early surveillance and oncogenesis intervening. Traditional cell-based models and animal-based models are unrealistic and unreliable for translational study, respectively ascribing to the limited tumor heterogeneity and species-related variation. Organoid emerged as a fidelity model that well preserves the properties of its origin. With inherent quality of holistic perspective, organoid is therefore ideally suited for delineating the carcinogenesis under risk exposure, in favor of understanding pathogen-host interactions and alleviating cancer initiation. In this review, we have summarized the organoid model-based evidence that identified or validated carcinogenic risks, mainly including diet, aging, microbial infection, and chemical exposure. In addition, we envisioned the exciting prospect of organoid model in screening promising treatment and/or prevention during tumorigenesis. As a robust 3D in vitro system, organoid has been widespread applied in basial and clinical cancer research, which may elucidate crucial mechanisms of oncogenesis and develop novel targeting strategies.     

Widening the window of persistence in seasonal pathogen-host systems

Local instability of exploiter-victim systems is well-known in both theory and in nature. Victims can be too sparse to support exploiter reproduction (under-exploitation) or they can be too readily driven to extinction (over-exploitation). Exploiters of seasonal resources face the additional challenge of surviving periods when victims are rare or unavailable. We formulate a fully stochastic model of highly seasonal pathogen-host dynamics and explore the interactions between an entomopathogenic nematode and its lepidopteran host. Our model suggests that if nematode populations experience the high rates of mortality predicted by short-term laboratory experiments, the paired threats of under- and over-exploitation should preclude the long-term persistence of this exploiter-victim system. We measured nematode mortality rates in the field and found that long-term mortality is lower than that predicted by short-term experiments. Incorporation of this new data into our model produces long-term persistence of local nematode populations across a range of initial nematode densities.     

Region-specific deposition of dermal proteins between dermis and epidermis during induction of chick feather and scale rudiments

To begin to study the role of particular proteins in inductive tissue interactions, we have used density labelling techniques to determine whether any dermal proteins are found between embryonic chick dermis and epidermis at a stage when the dermis plays an important inductive role in epidermal differentiation. Epidermis will form feathers or scales depending on whether it interacts with dorsal or foot dermis, respectively, and the dermis can still influence epidermal differentiation when direct cell contact between the tissues is blocked by a membrane filter during culturing (Peterson & Grainger, 1985). In transfilter experiments, we detect a subset of dermal proteins within the filter between the tissues. Several of these dermal proteins are deposited in a region-specific manner, that is, they are only found associated with filters from either dorsal or foot dermis. We have previously shown that the expression of some of these proteins is specific to particular regions of dermis and is also associated with the inductive potential of the dermis (Peterson & Grainger, 1986). We detect only 17 dermal proteins which are transferred across the filter in these cultures and found in direct association with epidermis; of these 14 are common to both dorsal and foot dermis, and 3 are deposited in a region-specific manner. Our results lead us to hypothesize a significant function for certain dermal proteins in this inductive interaction either as part of the extracellular matrix or in direct association with epidermis.     

The genome of the obligately intracellular bacterium Ehrlichia canis reveals themes of complex membrane structure and immune evasion strategies

Ehrlichia canis, a small obligately intracellular, tick-transmitted, gram-negative, alpha-proteobacterium, is the primary etiologic agent of globally distributed canine monocytic ehrlichiosis. Complete genome sequencing revealed that the E. canis genome consists of a single circular chromosome of 1,315,030 bp predicted to encode 925 proteins, 40 stable RNA species, 17 putative pseudogenes, and a substantial proportion of noncoding sequence (27%). Interesting genome features include a large set of proteins with transmembrane helices and/or signal sequences and a unique serine-threonine bias associated with the potential for O glycosylation that was prominent in proteins associated with pathogen-host interactions. Furthermore, two paralogous protein families associated with immune evasion were identified, one of which contains poly(G-C) tracts, suggesting that they may play a role in phase variation and facilitation of persistent infections. Genes associated with pathogen-host interactions were identified, including a small group encoding proteins (n = 12) with tandem repeats and another group encoding proteins with eukaryote-like ankyrin domains (n = 7).     

PHIDIAS: a pathogen-host interaction data integration and analysis system

The Pathogen-Host Interaction Data Integration and Analysis System (PHIDIAS) is a web-based database system that serves as a centralized source to search, compare, and analyze integrated genome sequences, conserved domains, and gene expression data related to pathogen-host interactions (PHIs) for pathogen species designated as high priority agents for public health and biological security. In addition, PHIDIAS allows submission, search and analysis of PHI genes and molecular networks curated from peer-reviewed literature. PHIDIAS is publicly available at .     

Genome-wide screen for temperature-regulated genes of the obligate intracellular bacterium, <Emphasis Type="Italic">Rickettsia typhi</Emphasis>

Background  

The ability of rickettsiae to survive in multiple eukaryotic host environments provides a good model for studying pathogen-host molecular interactions. Rickettsia typhi, the etiologic agent of murine typhus, is a strictly intracellular gram negative α-proteobacterium, which is transmitted to humans by its arthropod vector, the oriental rat flea, Xenopsylla cheopis. Thus, R. typhi must cycle between mammalian and flea hosts, two drastically different environments. We hypothesize that temperature plays a role in regulating host-specific gene expression, allowing R. typhi to survive in mammalian and arthropod hosts. In this study, we used Affymetrix microarrays to screen for temperature-induced genes upon a temperature shift from 37°C to 25°C, mimicking the two different host temperatures in vitro.     

Congenital cutaneous candidiasis associated with maternal peripartum candidemia

BackgroundCutaneous congenital candidiasis (CCC) is a rare condition consisting of invasive fungal infection of the epidermis and dermis that mostly affects preterm infants. Maternal vaginal candidiasis is present in half of the cases, although the occurrence of invasive candidiasis during pregnancy or peripartum period is exceptional.Case reportWe present the case of a full-term infant that was born by vacuum-assisted vaginal delivery to an apparently healthy 33 year-old woman with no history of intravenous drug use or vaginal candidiasis during pregnancy. The newborn showed a diffuse maculopapular rash with respiratory distress and bilateral interstitial lung infiltrates, requiring nasal continuous positive airway pressure support. Blood cultures obtained from the mother due to intrapartum fever yielded Candida albicans. Cultures of vaginal discharge and neonate skin also yielded C. albicans with the same in vitro susceptibly pattern. No alternative source for candidemia was identified. The clinical course after starting a systemic antifungal therapy was favorable in both the mother and the neonate, with clearance of candidemia and resolution of the skin lesions.ConclusionsCCC must be considered in full-term newborns with maculopapular rash at birth or during the first days of life. The absence of alternative sources for bloodstream infection in the present case suggests a potential etiopathogenic relationship between CCC and maternal candidemia. It is reasonable to rule out postpartum candidemia when CCC is suspected.     

Dimerization of inositol monophosphatase <Emphasis Type="Italic">Mycobacterium tuberculosis</Emphasis> SuhB is not constitutive,but induced by binding of the activator Mg<Superscript>2+</Superscript>

Background  

The cell wall of Mycobacterium tuberculosis contains a wide range of phosphatidyl inositol-based glycolipids that play critical structural roles and, in part, govern pathogen-host interactions. Synthesis of phosphatidyl inositol is dependent on free myo-inositol, generated through dephosphorylation of myo-inositol-1-phosphate by inositol monophosphatase (IMPase). Human IMPase, the putative target of lithium therapy, has been studied extensively, but the function of four IMPase-like genes in M. tuberculosis is unclear.