MicrobiologyBytes

Emerging pathogens cause new or previously unrecognized diseases, and among them, emerging zoonotic diseases are a major concern among scientists studying infectious diseases at different spatial and temporal scales. Changes in conditions may alter population disease dynamics and lead to the emergence of zoonotic infections. During the last decades, several outbreaks of emerging and re-emerging viral pathogens have occurred, affecting both purely-local and worldwide/pandemic involvement of human populations. Among the conspicuous examples are influenza A, Ebola virus, hepatitis C virus, severe adult respiratory distress (SARS), coronavirus, and human immunodeficiency virus, which challenge prevention and control measures of public health systems. In the Americas, the recent outbreak of pandemic influenza A subtype H1N1 became a major target for control due to its rapid spread, and uncertainties in virulence and transmissibility, yet vaccine availability was limited when significant activity occurred in advance of the traditional influenza season. However, in the last century outbreaks of several viral-related diseases have emerged or re-emerged involving arenaviruses and dengue viruses, and more recently, hantaviruses, and the expansion of the geographic range of West Nile virus. Among zoonotic diseases, small mammals are hosts of several pathogenic RNA viruses, especially Arenaviridae and Bunyaviridae.

Hantaviruses in the Americas and Their Role as Emerging Pathogens. Viruses. 2010; 2(12): 2559-2586. doi:10.3390/v2122559
The continued emergence and re-emergence of pathogens represent an ongoing, sometimes major, threat to populations. Hantaviruses (family Bunyaviridae) and their associated human diseases were considered to be confined to Eurasia, but the occurrence of an outbreak in 1993–94 in the southwestern United States led to a great increase in their study among virologists worldwide. Well over 40 hantaviral genotypes have been described, the large majority since 1993, and nearly half of them pathogenic for humans. Hantaviruses cause persistent infections in their reservoir hosts, and in the Americas, human disease is manifest as a cardiopulmonary compromise, hantavirus cardiopulmonary syndrome (HCPS), with case-fatality ratios, for the most common viral serotypes, between 30% and 40%. Habitat disturbance and larger-scale ecological disturbances, perhaps including climate change, are among the factors that may have increased the human caseload of HCPS between 1993 and the present. We consider here the features that influence the structure of host population dynamics that may lead to viral outbreaks, as well as the macromolecular determinants of hantaviruses that have been regarded as having potential contribution to pathogenicity.

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• Unknown disease in South Africa identified as arenavirus infection
• A new arenavirus associated with hemorrhagic fever
• Where do viruses come from?

SciReadr.com is based on the reading list for students the School of Biological Sciences at the University of Leicester. We know that students don’t read the books we suggest on the reading list, so the University of Leicester Student Experience Enhancement Group funded Project SOAR, which has two parts.

The first is SciReadr.com, an interactive site where you can browse, rate, review, borrow or buy the books on the reading list. If you’d like to know more, there’s lots of information here. We’re also on Facebook and Friendfeed if that’s easier for you, and we’d like hear any suggestions you have about the website.

Scireadr.com is open to everyone, but if you have a University of Leicester email address, after you’ve read a book, you can come along to a Book Group meeting in the Student’s Union, pick up a coffee from Starbucks or a beer from the bar and spend a happy couple of hours chatting with people who’ve read the same book. Sound interesting? The first book group meeting is in February and the book we’ll be discussing is Bill Bryson’s A Short History of Nearly Everything, so if you’re interested and have a University of Leicester email address, sign up at SciReadr.com now.

Candida albicans is the predominant fungal pathogen of humans. In healthy individuals C. albicans is a commensal inhabitant of the gastrointestinal, oral and vaginal tracts. C. albicans can cause superficial infections which, although not life threatening, provide discomfort to the individual and require treatment with antifungals which is a constant drain on hospitals resources. However, C. albicans infections are life threatening when the individual’s immune system becomes compromised as a result of age, cancer, chemotherapy hospitalisation and AIDS. Under these circumstances superficial infections may readily develop into systemic disease where mortality rates are reported to be up to 40%, which is higher than those for most bacterial infections.

Pathogenic microorganisms can produce a variety of secondary metabolites and signalling molecules which can affect the host, or provide them with a selective advantage against competing commensal organisms. This paper demonstrates that gaseous, metabolically generated CO₂ can serve as a signalling molecule to enhance the organism’s virulence during infection establishment by using the fungal pathogen Candida albicans as a model. The researchers identified a CO₂ receptor site within the catalytic domain of the soluble adenylyl cyclase, Cyr1p, which is critical for CO₂ sensing and hence virulence of the organism. CO₂ sensing is conserved in a variety of pathogenic species, and increased levels have been shown to suppress the host’s immune system. CO₂ sensing may represent a mechanism to enhance C. albicans virulence when the host’s immune system is suppressed.

CO₂ Acts as a Signalling Molecule in Populations of the Fungal Pathogen Candida albicans. (2010) PLoS Pathog 6(11): e1001193. doi:10.1371/journal.ppat.1001193
When colonising host-niches or non-animated medical devices, individual cells of the fungal pathogen Candida albicans expand into significant biomasses. Here we show that within such biomasses, fungal metabolically generated CO₂ acts as a communication molecule promoting the switch from yeast to filamentous growth essential for C. albicans pathology. We find that CO₂-mediated intra-colony signalling involves the adenylyl cyclase protein (Cyr1p), a multi-sensor recently found to coordinate fungal responses to serum and bacterial peptidoglycan. We further identify Lys 1373 as essential for CO₂/bicarbonate regulation of Cyr1p. Disruption of the CO₂/bicarbonate receptor-site interferes selectively with C. albicans filamentation within fungal biomasses. Comparisons between the Drosophila melanogaster infection model and the mouse model of disseminated candidiasis, suggest that metabolic CO₂ sensing may be important for initial colonisation and epithelial invasion. Our results reveal the existence of a gaseous Candida signalling pathway and its molecular mechanism and provide insights into an evolutionary conserved CO₂-signalling system.

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• New Mechanism Fundamental to the Spread of Invasive Yeast
• Statins and Candida