MicrobiologyBytes

MicrobiologyBytes has discussed before Craig Venter’s attempts to create a synthetic microorganism. In 2008, Venter described his work at the TED Conference, and his talk is well worth watching:

Related:

• Mycoplasma laboratorium, the first synthetic organism
• The end of the world? Dr Franken-Venter?

There are many descriptions of bacterial genes that have been found within nematode and arthropod chromosomes. In this article in Microbiology Today, Julie Dunning Hotopp and Jason Rasgon explain how they got there:

The arthropod-infecting Wolbachia exert unusual effects on host reproduction, including parthenogenesis, whereby infected virgin females produce infected female offspring, male killing, whereby infected male embryos fail to develop, feminization, whereby genetic males develop into reproductively capable females, and cytoplasmic incompatibility, the most common phenotype, whereby the offspring of uninfected females and infected males fail to develop. Wolbachia are maternally inherited, being transferred through the egg cytoplasm. Therefore, these reproductive phenotypes favouring Wolbachia-infected females increase the proliferation of Wolbachia-infected arthropods. Wolbachia are parasitic endosymbionts, since the interaction benefits Wolbachia while exerting a negative effect on the host by limiting genetic exchange. However, a mutualistic role benefiting both organisms cannot be excluded.

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Related:

• Wolbachia

Melioidosis is a severe disease affecting humans and animals in the tropics. It is caused by the bacterium Burkholderia pseudomallei, which lives in tropical soil and especially occurs in southeast Asia and northern Australia. Despite the recognition that melioidosis is an emerging infectious disease, little is known about the habitat of B. pseudomallei in the environment.

Researchers from Menzies School of Health Research in Darwin, Australia have found that the soil bacterium Burkholderia pseudomallei, which causes the emerging infectious disease melioidosis in humans and animals, is associated with land management changes such as livestock husbandry or residential gardening. They performed a survey in the Darwin area in tropical Australia, screening 809 soil samples for the presence of these bacteria using molecular methods. The study sheds light on the environmental occurrence of this bacterium in the soil.

B. pseudomallei lives in tropical soil and is endemic in southeast Asia and northern Australia, where it can be a common cause of fatal community-acquired bacterial pneumonia. In predisposed hosts such as those with diabetes, it can also lead to systemic sepsis, with mortality rates over 50 percent. Through a large survey in the tropical Darwin area of Australia, the authors found that environmental factors describing the habitat of these bacteria differed between environmentally undisturbed and disturbed sites. At undisturbed sites, B. pseudomallei was primarily found in close proximity to streams and in grass- and roots-rich areas. In disturbed soil, B. pseudomallei was associated with the presence of animals, farming or irrigation. Highest B. pseudomallei counts were retrieved from paddocks, pens and kennels holding livestock and dogs. This study contributes to the elucidation of the habitat of B. pseudomallei in northern Australia. It also raises concerns that B. pseudomallei may spread due to changes in land management.

These findings raise concerns that B. pseudomallei may spread due to the influence of land management changes. This would increase the risk of human and livestock exposure to these potentially deadly bacteria which are transmitted by contact with contaminated soil or surface water through cuts in the skin or inhalation. In-depth analysis of the influence of anthropogenic factors upon B. pseudomallei and further studies in other endemic areas are needed to confirm the results of this study.

Landscape Changes Influence the Occurrence of the Melioidosis Bacterium Burkholderia pseudomallei in Soil in Northern Australia. PLoS Negl Trop Dis 3(1): e364

Related:

• Glanders and Melioidosis – coming soon to a crowded shopping centre near you?

Sleep quality is thought to be an important predictor of immunity and, in turn, susceptibility to the common cold. A new article examines whether sleep duration and efficiency in the weeks preceding virus exposure are associated with cold susceptibility. A total of 153 healthy men and women (age range, 21-55 years) volunteered to participate in the study. For 14 consecutive days, they reported their sleep duration and sleep efficiency (percentage of time in bed actually asleep) for the previous night and whether they felt rested. Average scores for each sleep variable were calculated over the 14-day baseline. Subsequently, participants were quarantined, administered nasal drops containing a rhinovirus, and monitored for the development of a clinical cold (infection in the presence of objective signs of illness) on the day before and for 5 days after exposure.
Results: There was a graded association with average sleep duration: participants with less than 7 hours of sleep were 2.94 times more likely to develop a cold than those with 8 hours or more of sleep. The association with sleep efficiency was also graded: participants with less than 92% efficiency were 5.50 times more likely to develop a cold than those with 98% or more efficiency. These relationships could not be explained by differences in prechallenge virus-specific antibody titers, demographics, season of the year, body mass, socioeconomic status, psychological variables, or health practices. The percentage of days feeling rested was not associated with colds.
Conclusion: Poorer sleep efficiency and shorter sleep duration in the weeks preceding exposure to a rhinovirus were associated with lower resistance to illness.

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Sleep habits and susceptibility to the common cold. 2009 Arch Intern Med. 169(1): 62-67

Related:

• Bacteria can sense when we are stressed
• Dirty Money

Transmission of Plasmodium, the causative agent of malaria, requires the completion of a complex life cycle in the mosquito, which includes invasion of the salivary glands. This invasion depends on the recognition of mosquito salivary gland surface components by the parasite. Malaria is estimated to infect 300 to 500 million people worldwide resulting in over 1 million deaths each year.

Researchers have now identified the molecular components that enable the malaria-causing parasite Plasmodium to infect the salivary glands of the Anopheles mosquito – a critical stage for spreading malaria to humans. Saglin, a mosquito salivary protein, is a receptor for the Plasmodium protein Thrombospondin-Related Anonymous Protein (TRAP). The two proteins bind together to allow invasion of the salivary gland by Plasmodium sporozoites, which can be transmitted to a human when bitten by an infected mosquito. Through a series of experiments, the scientists found that saglin bound with the artificial peptide SM1. The team then developed an antibody to find a protein similar to SM1 that existed naturally in the parasite, which they identified as TRAP. To further prove the interaction between saglin and TRAP, the team conducted experiments to down-regulate, or switch off, saglin expression, which greatly diminished salivary gland invasion in the mosquito. This work is the culmination of a decade-long research project in which peptide libraries were used to understand the mechanisms that the parasite uses to develop in its obligatory mosquito host, and demonstrates that interaction between the salivary-gland-specific surface protein saglin and the parasite surface protein TRAP is essential for invasion to occur. A better understanding of the mechanisms used by the parasite to develop in the mosquito may lead to novel approaches to intervene with the spread of the disease.

Malaria Parasite Invasion of the Mosquito Salivary Gland Requires Interaction between the Plasmodium TRAP and the Anopheles Saglin Proteins. 2009 PLoS Pathog 5(1): e1000265
SM1 is a twelve-amino-acid peptide that binds tightly to the Anopheles salivary gland and inhibits its invasion by Plasmodium sporozoites. By use of UV-crosslinking experiments between the peptide and its salivary gland target protein, we have identified the Anopheles salivary protein, saglin, as the receptor for SM1. Furthermore, by use of an anti-SM1 antibody, we have determined that the peptide is a mimotope of the Plasmodium sporozoite Thrombospondin Related Anonymous Protein (TRAP). TRAP binds to saglin with high specificity. Point mutations in TRAP’s binding domain A abrogate binding, and binding is competed for by the SM1 peptide. Importantly, in vivo down-regulation of saglin expression results in strong inhibition of salivary gland invasion. Together, the results suggest that saglin/TRAP interaction is crucial for salivary gland invasion by Plasmodium sporozoites.

Related:

• MicrobiologyBytes: Malaria
• Malaria, mosquitoes and the legacy of Ronald Ross
• New ways to beat malaria
• Researchers characterize potential protein targets for malaria vaccine
• Gametogenesis in malaria parasites

Bees are important contributors to the economies of many countries, but as Travis Glare and Maureen O’Callaghan discuss in this article in Microbiology Today, they are many threats to the survival on the humble bee, including the risk of disease from micro-organisms:

There are many threats to bee survival, including the risk of disease caused by micro-organisms. The vast majority of our knowledge of bee diseases focuses on the honey bee, Apis mellifera, although there are actually over 20,000 species, both stingless and stinging, from those with solitary lifestyles to complex societies such as honey bee hives. Viruses, fungi, protozoa and bacteria are all known to cause infections in bees, sometimes leading to collapse of colonies, and causing serious threats to the bee-keeping industry. Bees have two distinct life forms, brood (egg, larva and pupal stages which develop within the hive) and adult. Most diseases are specific to just one of these life stages. While the list of diseases is quite long, only a few are of serious concern to apiculturists.

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Related:

• Colony Collapse Disorder
• The great bee swindle – colony collapse disorder

Nice microbiology video from the Royal Sussex County Hospital NHS Trust.

discovermagazine.com

It was just a matter of time before someone discovered that Madagascar is a museum for viruses. The discovery came when a team of American and English scientists perused the genome of the gray mouse lemur. Nestled among its genes were segments of DNA that bore a remarkable resemblance to HIV. How on Earth could a deadly virus’s genes become part of a primate’s own genome? Some kinds of viruses, known as retroviruses, replicate by inserting their DNA into host cells, where their DNA can guide the production of new viruses. But many studies indicate that sometimes these viruses infect the cells that will give rise to sperm and eggs. The virus ends up in a fertilized egg and gets passed down to ever cell in the developing embryo–including its own sex cells. Now the virus gets passed down through the generations. It may still retain the ability to infect other cells for a while, but mutations typically knock out that ability. Instead, the virus can only insert copies of its DNA back into its own host cell’s genome. Over millions of years, this viral DNA spreads through the host genome. Our own DNA contains 98,000 stretches of this virus DNA, plus 150,000 tiny viral fragments, making up about 8% of our genome – about five times more DNA than the DNA that encodes proteins.

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Related:

• Phoenix from the ashes: The 5 million year old virus

I recently spent some time as a patient on a ward in an NHS hospital where I had been admitted for some tests. Thankfully, all the results were negative and I was diagnosed as being quite healthy for a person of my advanced age :-)

As anyone who has ever spent any time as an NHS patient knows only too well, one of the defining features of the experience is an awful lot of waiting around. I spent just under a day on a Clinical Decisions Unit ward where patients are admitted for testing and then either discharged or moved on to longer stay wards for treatment. There were a lot of very sick people on the ward, but I was feeling fine, so there wasn’t much I could do other than sit and observe the goings on, which is how I discovered that

Infection control in hospitals is broken

“Hospital superbugs” such as Staphylococcus aureus MRSA, Clostridium difficile and Noroviruses feature prominently in the news media and consequently on MicrobiologyBytes, with claim and counterclaim about increasing, static or declining infection rates constantly being batted backwards and forwards, and the Department of Health publishes endless guidance on infection control procedures. Apart from quack claims of miracle cures, the formal response to hospital-acquired infections are procedures for infection control such as cleaning, disinfection and sterilization, protective equipment and surveillance of infection rates. As an observer on a busy ward I was able to watch what happened as patients and staff came and went.

The care I received was exemplary, and for the most part, the ancillary, nursing and medical staff worked hard and clearly cared about the welfare of the patients. But that’s not enough. The reality is that the complexity of the system pushed all the staff beyond their limits, and damaged morale. As a simple example, I watched a domestic ancillary employed as bed maker drifting around looking for beds to make. She was once about to make one when she was called away, and when she came back, the nurses had made the bed. I listened to the nurses grumble about how the ancillaries didn’t do their jobs properly, and the ancillaries grumble about the nurses. And of course, everyone grumbled about the medical staff. Morale was at a low ebb. But it gets worse. Time and time again I watched ward staff strip the linen from beds which had been vacated by patients and painstakingly disinfect the mattress and the bed before remaking the bed with fresh linen. What’s wrong with that? No-one cleaned the bedside chairs. When the next patient arrived, they kicked their bags around on the floor for a while before putting them on the chair, which the nurses dumped the fresh linen on before making the beds.

In less than 24 hours, I was treated by dozens of medical staff and wheeled all over the hospital for various tests. The ward was like a motorway, with staff, patients and visitors constantly moving from ward to ward, street to common areas, canteens and homes. Flawed understanding of basic microbiology is not compensated for by mandated infection control procedures rigidly-applied without any thought or appreciation. Errors are compounded by a totemic belief in the miracle properties of alcohol hand rubs which adorn every bed but which distract from more effective handwashing procedures. Did I need to be visited by the person flitting from ward to ward to fiddle with the TV/radio/phone console above every bed? Even if they did spend several seconds squirting alcohol gel on their hands before moving on to the next patient? I don’t think so.

Infection control in hospitals is broken by the complexity of the system

So how can you fix it? Apart from better microbiology training, the system needs to be radically simplified so that staff and patients are not constantly moving around. Wards should be much more autonomous with a limited number of staff responsible for them, and allowed to do their jobs properly. This would allow much better standards of care arising from the evident motivation they have. There’s no need for people to flit constantly from ward to ward, delivering meals, borrowing equipment, chasing test results and spreading contamination. Simplify. Let people do the jobs they have been trained for and to feel pride in themselves. Back to basics.

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