MicrobiologyBytes

Bacterial communities often synthesize and embed themselves in a sticky polymer matrix known as a biofilm which provides a safe environment protected from many environmental stresses. As Steve Atkinson describes in this article in Microbiology Today, for this mode of living to be successful the members of the community need to communicate:

When the first bacteria were observed with a microscope, it must have been something of a leap of faith to believe they were living organisms, let alone consider that they were not behaving as individuals, but were in fact co-operating in a coordinated community where cell-to-cell communication plays an integral part in their life cycle. As early as 1905, Erwin Frink Smith, in his manuscript Bacteria in relation to plant disease was astute enough to comment that ‘a multiple of bacteria are stronger than a few’, but it was not until the early 1990s that the concept of bacterial cell-to-cell communication actually gained credence within the microbiological community with the discovery that bacteria employ chemical signals (pheromones) to communicate, and so coordinate population-wide behaviour with changes in environmental conditions. The concept of bacterial cell-to-cell signalling, usually referred to as quorum sensing (QS), has now been observed in a wide variety of Gram-positive and Gram-negative plant and animal pathogens, including those responsible for important human diseases. It is also noteworthy that QS systems are not limited to prokaryotes, but have also been described in eukaryotes such as yeast.

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The risk of tuberculosis (TB) and latent TB (in which the bacteria that cause TB lie dormant but can reactivate later to cause active TB disease) is higher in the prison population than in the general population. And importantly, the spread of TB and latent TB within prisons can substantially increase their incidence in the general population. These findings suggest that improvements in prison TB control would not only help to protect prisoners and staff from within-prison spread of TB, but would also reduce national TB burdens. Using previous findings from published studies and data from the World Health Organization, the authors calculated the ratio between the incidence rates for TB and latent TB in prison and in the general population. The average incidence of TB in prisons was 23 times higher that of the general population, and for latent TB, was 26 times higher in prisons than in the general population. The authors also estimated the fraction of TB in the general population attributable to within-prison exposure to TB and found that, on average, the population attributable fraction for TB in high-income countries was 8.5%; in middle-to-low–income countries, the average the population attributable fraction for TB was 6.3%.

The authors say: “These data may prove useful to inform the development of rational policies to control TB transmission in correctional facilities.” They add: “Future studies should assess the population attributable risk of prison-to-community spread and describe the conditions in the prison that influence TB transmission.” In an accompanying editorial, the PLoS Medicine editors conclude: “The publication of this systematic review marks a shift from considering the incidence of TB in each prison population to considering the massive global impact of tuberculosis in prisons.”

Tuberculosis Incidence in Prisons: A Systematic Review. (2010) PLoS Med 7(12): e1000381.doi:10.1371/journal.pmed.1000381

Related:

1. Why is TB more common in men than in women?
2. Origin and spread of Mycobacterium tuberculosis
3. Tuberculosis – is the white plague winning?

The mitochondrion lies at the heart of eukaryotic cell biology, with key roles in energy production, apoptosis, free radical biology and intermediary metabolism. Fully integrated into the life of the cell, it functions as a subcellular organelle, but its origins lie elsewhere. As long ago as 1890, German cell biologist Richard Altmann proposed that mitochondria were autonomous elemental life forms, similar to bacteria. In the first half of the 20th century, a number of investigators made similar links between mitochondria and bacteria. However, it was only with the discovery of mitochondrial DNA (mtDNA) in the 1960s that the idea that mitochondria were derived from bacteria gained wider acceptance, particularly in the context of the serial endosymbiotic theory that proposed that the eukaryotic cell originated from multiple prokaryotic precursors. Although some components of this theory have been abandoned (e.g. spirochaetes as precursors of eukaryotic cilia and flagella), evidence for and acceptance of the endosymbiotic origins of mitochondria have accumulated steadily over the past half century and numerous extensive and deep similarities are now recognised between mitochondria and their bacterial relatives. Most microbiologists and cell biologists are probably already aware of the fact that mitochondria are now considered descendents of endosymbiotic bacteria and they are comfortable with this description of the facts. However, the way we describe the world influences the way we think about it, so what if we abandon caution and state simply that mitochondria are bacteria and see where this reformulation leads us?

Time to recognise that mitochondria are bacteria? Trends Microbiol. Nov 29 2010
The scientific community is comfortable with recognising mitochondria as organelles that happen to be descendants of bacteria. Here, I playfully explore the arguments for and against a phylogenetic fundamentalism that states that mitochondria are bacteria and should be given their own taxonomic family, the Mitochondriaceae. I also explore the consequences of recognizing mitochondria as bacteria for our understanding of the systemic response to trauma and for the prospects of creating transgenic mitochondria.

Related:

• Microbial Mitopathogens
• Yeast shows what drives cells to divide

We know of a large number of diseases or medical conditions that affect humans more severely than non-human primates. Humans are more sensitive than chimpanzees to the severe effects of certain virus infections, such as progression of HIV to AIDS or severe complications from hepatitis B. These differences likely arise from different immune responses to infection among species. However, due to the lack of comparative functional data across species, it remains unclear how the immune system of humans and other primates differ.

This paper present the first genome-wide characterization of functional differences in innate immune responses between humans and our closest evolutionary relatives. The results indicate that “core” immune responses, those that are critical to fight any invading pathogen, are the most conserved across primates and that much of the divergence in immune responses is observed in genes that are involved in response to specific microbial and viral agents. Human-specific immune responses are enriched for genes involved in apoptosis and cancer biology, as well as with genes previously associated with susceptibility to infectious diseases or immune-related disorders. Finally, it shows that chimpanzee-specific immune signaling pathways are enriched for HIV–interacting genes. These observations may help explain known inter-species differences in susceptibility to infectious diseases. Though detailed species-specific gene expression patterns were identified in this study, more experiments will be required to assess the phenotypic impact of those unique immune responses. Future studies will also test the immune response of each species to specific infectious agents. This is only the first step in characterizing inter-species differences in immune response.

Functional Comparison of Innate Immune Signaling Pathways in Primates. (2010) PLoS Genet 6(12): e1001249. doi:10.1371/journal.pgen.1001249
Humans respond differently than other primates to a large number of infections. Differences in susceptibility to infectious agents between humans and other primates are probably due to inter-species differences in immune response to infection. Consistent with that notion, genes involved in immunity-related processes are strongly enriched among recent targets of positive selection in primates, suggesting that immune responses evolve rapidly, yet providing only indirect evidence for possible inter-species functional differences. To directly compare immune responses among primates, we stimulated primary monocytes from humans, chimpanzees, and rhesus macaques with lipopolysaccharide (LPS) and studied the ensuing time-course regulatory responses. We find that, while the universal Toll-like receptor response is mostly conserved across primates, the regulatory response associated with viral infections is often lineage-specific, probably reflecting rapid host–virus mutual adaptation cycles. Additionally, human-specific immune responses are enriched for genes involved in apoptosis, as well as for genes associated with cancer and with susceptibility to infectious diseases or immune-related disorders. Finally, we find that chimpanzee-specific immune signaling pathways are enriched for HIV–interacting genes. Put together, our observations lend strong support to the notion that lineage-specific immune responses may help explain known inter-species differences in susceptibility to infectious diseases.

Related:

• Genomic fossils in lemurs shed light on HIV
• You Are Not What You Eat

Recent events have highlighted the damage our dependence on oil can wreak on the natural world. However, as Lena Ciric discusses in this article in Microbiology Today, communities of bacteria have evolved over billions of years to be rather better than we are at breaking down the complex hydrocarbons that are found in oil. How we can exploit this ability to improve our future clean-up strategies?

On 20th April 2010 a massive explosion rang out in the Gulf of Mexico. The source of the incident was the Deepwater Horizon drilling rig, situated about 84 km from the Louisiana coast, which had been drilling for oil at a depth of over 1,500 m. The explosion killed 11 people at the time and was the cause of what is now referred to as the worst environmental disaster in US history. It is difficult to state the exact volume of oil which has spilled into the Gulf of Mexico, the best estimate being put forward by the US government as 4.9 million barrels. That’s over 770 million litres, or over 300 full Olympic-size swimming pools. The well which was the source of the oil spill has since been plugged successfully and a US government report has stated that three-quarters of the spilled oil as now been ‘dealt with’. A considerable proportion of the removal of the spill is attributed to bacterial biodegradation of the hydrocarbons that constitute the crude oil. The huge oil spill in the Gulf of Mexico is only one of a huge number of oil spills that have taken place over the course of Earth’s history. For billions of years, our microbial neighbours have been evolving to utilize the molecules that constitute oil – and it turns out that they have now become quite
good at it.

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Related:

• Molecular approaches to bioremediation

From the outside and within, we are constantly bombarded with a myriad of diverse microbial species. However, our bodies are equipped with an evolutionarily conserved innate immune defense system that allows us to thwart potential pathogens. Antimicrobial peptides (AMPs) are a unique and assorted group of molecules produced by living organisms of all types, considered to be part of the host innate immunity. These peptides demonstrate potent antimicrobial activity and are rapidly mobilized to neutralize a broad range of microbes, including viruses, bacteria, protozoa, and fungi. More significantly, the ability of these natural molecules to kill multidrug-resistant microorganisms has gained them considerable attention and clinical interest. With the growing microbial resistance to conventional antimicrobial agents, the need for unconventional therapeutic options has become urgent. This article provides an overview of AMPs, their biological functions, mechanism of action, and applicability as alternative therapeutic agents.

Presently, AMPs represent one of the most promising future strategies for combating infections and microbial drug resistance. This is evident by the increasing number of studies to which these peptides are subjected. As our need for new antimicrobials becomes more pressing, the question remains: can we develop novel drugs based on the design principles of primitive molecules?

Antimicrobial Peptides: Primeval Molecules or Future Drugs? (2010) PLoS Pathog 6(10): e1001067. doi:10.1371/journal.ppat.1001067

Related:

• Antimicrobial Peptides
• Antimicrobial Peptides: Primeval Molecules or Future Drugs?
• How to avoid getting killed

The term ‘endocytosis’ includes at least four mechanisms: phagocytosis, macropinocytosis, clathrin mediated endocytosis, and caveolin mediated endocytosis, which differ in several properties such as vesicular size, markers and regulation. Different viruses use cellular endocytic mechanisms to enter and infect cells with the clathrin mediated pathway being the most commonly observed uptake pathway. Once HIV is internalized, virus particles can follow different pathways: they can be secreted (as in the case of transcytosis) or degraded, or they can fuse with vesicular membranes to inject the viral core into the cytoplasm and initiate the viral infection cycle. However, the exact contribution of endocytic pathways to the infection of CD4+ T lymphocytes and to HIV pathogenesis in vivo is mostly unknown, and the mechanisms governing endocytosis also remain unclear. This paper discusses recent developments in the study of HIV entry and the different experimental approaches that have caused the role of endocytic pathways in HIV infection to be revisited, with the aim of updating and formulating new perspectives in the field of HIV entry.

Endocytosis of HIV: anything goes. (2010) Trends Microbiol. 18(12): 543-551
The major pathway for HIV internalization in CD4+ T cells has been thought to be the direct fusion of virus and cell membranes, because the cell surface is the point of entry of infectious particles. However, the exact contribution of endocytic pathways to the infection of CD4+ T lymphocytes is unknown, and the mechanisms involved in endocytosis of HIV particles are unclear. Recent evidence suggests that endocytosis of cell-free and cell-associated virus particles could lead to effective virus entry and productive infections. Such observations have, in turn, spurred a debate on the relevance of endosomal entry as a mechanism of escape from the immune system and HIV entry inhibitors. In this paper, we review the endocytosis of HIV and discuss its role in HIV infection and pathogenesis.

Related:

• HIV-1 Entry, Inhibitors, and Resistance
• How HIV Infects Cells – The Entry Claw (Video)

One of humanity’s drives is to make things, allied with the curious desire to want to make them larger or smaller. On the small side of this equation, the science of nanotechnology attracts people with audacious dreams. Nanotechnologists want to fabricate the tiniest structures possible or, even better, the tiniest possible machines. The overarching desire is to create molecular sized devices of strictly defined dimensions, with little variation among the new entities, and to be able to produce multitudes over and over with few failures. Of course, bacteria have been doing this for some billions of years. Despite intermittent progress, only in the last decade have we begun to understand in any real depth how they do so.

The question that dominated discussion in this field 15–20 years ago was, How does a bacterium find its middle? That question seems well on its way to being answered. The new fundamental question about bacterial shape is, How does a bacterium construct a cell having a defined length, diameter, and overall geometry? Technical and genetic advances have finally made this question amenable to experiment and have reinvigorated the application of new forms of microscopic visualization.

Bacterial shape: two-dimensional questions and possibilities. (2010) Annu Rev Microbiol. 64: 223-240
Events in the past decade have made it both possible and interesting to ask how bacteria create cells of defined length, diameter, and morphology. The current consensus is that bacterial shape is determined by the coordinated activities of cytoskeleton complexes that drive cell elongation and division. Cell length is most easily explained by the timing of cell division, principally by regulating the activity of the FtsZ protein. However, the question of how cells establish and maintain a specific and uniform diameter is, by far, much more difficult to answer. Mutations associated with the elongation complex often alter cell width, though it is not clear how. Some evidence suggests that diameter is strongly influenced by events during cell division. In addition, surprising new observations show that the bacterial cell wall is more highly malleable than previously believed and that cells can alter and restore their shapes by relying only on internal mechanisms.

Related:

• Getting bacteria into shape
• Cell shape and cell-wall organization in Gram-negative bacteria
• Peptidoglycan – the strength and weakness of bacteria

Bacteriophages represent one of the most abundant biological entities in nature and have long been recognized for their potential use as therapeutic agents. In recent years overprescription of antibiotics and the concomitant development of antibiotic-resistant ‘super-bugs’ have highlighted the need for alternative strategies to combat infectious diseases. Consequently, a lot of phage research in the past two decades was aimed at assessing whether phage can be used to eliminate undesirable bacteria. Traceability is a requirement in modern food production, incorporating every step in the production process, commonly known as the ‘farm to fork’ concept (European Commission White paper on Food Safety, January 2000). Phages are omnipresent and are accidentally, yet regularly, consumed through ingestion of water and food. For this reason they are presumed to be safe as undesirable effects have not been reported. This, together with their specificity, makes them excellent tools for food safety purposes.

The ‘farm to fork’ concept identifies quality assurance steps at which bacterial contamination may occur, and which also represent critical points where phage treatments may be applied. The most frequently encountered food pathogens belong to one of the four dominant genera, Salmonella, enterotoxigenic Escherichia coli, Campylobacter and Listeria, along with less common infections by Clostridium spp., Staphylococcus aureus, Streptococcus suis and Cronobacter sakazakii. Phages targeting strains of each of these species have been identified and this review discusses the pros and cons of the use of phages as biocontrol, biosanitation and detection agents.

Bacteriophages as biocontrol agents of food pathogens. Curr Opin Biotechnol. Nov 4 2010
Bacteriophages have long been recognized for their potential as biotherapeutic agents. The recent approval for the use of phages of Listeria monocytogenes for food safety purposes has increased the impetus of phage research to uncover phage-mediated applications with activity against other food pathogens. Areas of emerging and growing significance, such as predictive modelling and genomics, have shown their potential and impact on the development of new technologies to combat food pathogens. This review will highlight recent advances in the research of phages that target food pathogens and that promote their use in biosanitation, while it will also discuss its limitations.

Related:

• Bugs Against Biofilms
• Bacteriophages for plant disease control
• 10 things you should know about E. coli O157