Key host–pathogen interactions for designing novel interventions against Helicobacter pylori

Helicobacter pylori is a Gram-negative bacterium which has exquisitely adapted to survive in the acidic, hostile environment of the stomach. H. pylori is extremely motile and is found in the mucus layer lining the stomach. By penetrating this thick mucus layer, the bacteria can attach to gastric epithelial cells, thus avoiding being ‘washed’ through the stomach. H. pylori infection tends to persist for the life of the host and, with more than half the population of the world being infected, it is not surprising that H. pylori strains have co-evolved with Homo sapiens. For this reason, and due to several cunning adaptations, the bacteria are able to induce low-level inflammation to gain access to the nutrients required for them to grow and survive, but simultaneously evade host immune responses. Importantly, H. pylori is presently the only bacterial species classified as a type 1 carcinogen by the World Health Organization (WHO) and remains a significant cause of morbidity and mortality worldwide. Approximately one in five infected individuals develop disease, including either peptic ulcer disease, gastric mucosal-associated lymphoid tissue lymphoma and, in the worst case (approximately 1–2% of infected individuals), gastric adenocarcinoma. Gastric cancer remains the second leading cause of death from malignancy worldwide and, with H. pylori being a major cause, it is clear that H. pylori infection still has a major impact on the global disease burden. Clearly there is a need to develop novel therapies and, ideally, a highly efficacious vaccine, based on a sound understanding of H. pylori and its interplay with the human host. This review will summarize recent findings in the context of host–pathogen interactions and modulation of inflammation as well as highlighting recent advances in vaccine development.

Every, A.L (2013) Key host–pathogen interactions for designing novel interventions against Helicobacter pylori Trends in Microbiology, 21, 253–259.

Don't touch?

Next time you enter a new hotel room, you might think twice before touching the light switch or reaching for the remote. Those are two of the top surfaces most likely to be contaminated with bacteria, according to a study aimed at boosting hotel cleaning practices.

For more see: http://vitals.msnbc.msn.com/_news/2012/06/17/12241651-germiest-hot-spots-in-hotels-tv-remote-light-switch-study-finds?chromedomain=testblog

Your Computer Mouse Carries More Germs Than A Toilet Seat

The average computer mouse is three times dirtier than a toilet seat, according to an alarming new study.
Researchers blame the results on  workers who eat at their desks, turning work stations into breeding grounds for harmful bugs and germs. And men are far more filthy than their female counterparts - with 40 per cent more bacteria lurking in male mice.Keyboards were the second most grubby item in the office, ahead of phones and chairs.Initial Washroom Hygiene, which carried out the tests, said computer mice also carried twice as many bugs as a toilet flush handle.
Researchers swabbed 158 items seized from 40 desks at three office locations and compared the results with data on toilet hygiene, including 28 loo seats, obtained from other buildings. Four-in-10 desks were home to at least one item with very high levels of bacteria and surface contamination which posed a risk to health.
Initial Technical manager Peter Barratt said: 'It is now common for office workers to spend their lunch hour eating at their desk - often surfing the web or continuing to type at the same time.
'This leaves crumbs and other food residue all over the work station, particularly on mice and keyboards, making them ideal places for bacteria and other microorganisms to survive and multiply.
'In addition because they are electrical devices these items aren’t cleaned as regularly or as thoroughly as other parts of the office, or even as the desks themselves.'
The mouse isn't the only everyday item found to be filthier than the average toilet seat - research has discovered more bacteria on kitchen work surfaces, steering wheels, restaurant high chairs, shopping trolleys and even lift buttons.
–Daily Mail, London

Antibiotic resistance: we must act now says WHO.

http://www.nhs.uk/news/2012/03march/Pages/antibiotic-resistance-who-strategy.aspx

Staphylococcus aureus might be an intracellular pathogen

Increasing evidence indicates that Staphylococcus aureus might be a facultative intracellular pathogen. In particular, certain subpopulations, called small colony variants (SCVs), seem to be well adapted to the intracellular milieu. When compared to ‘normal’ staphylococcal strains, SCVs show increased uptake by host cells, resistance to intracellular defences and reduced stimulation of host defences. We propose that the ability to form two subpopulations with different phenotypes might allow S. aureus the option for both extra- cellular and intra-cellular survival in the host.
Trends in Microbiology 2012 (Article in Press)

http://images.cell.com/images/Edimages/chom/TIM_Feb.pdf

Gene could be factor in frequent cold sores

People who get frequent flare-ups of cold sores may have variations of an obscure gene, according to a study published this week in the Journal of Infectious Diseases. This is the first gene to be associated with cold sore outbreaks.
Cold sores are the lesions caused by herpes simplex virus type 1, a persistent and common virus. The sores usually appear on the lip, around the mouth and sometimes on the nose, chin and fingers. Apart from the distress the sores can cause by their appearance, they can be painful and stick around for two weeks.
The sores also are infectious. Once a person has the virus, there’s no cure or way to predict or prevent the cold sores. The virus remains in the body and then unpredictably flares up in an outbreak of sores.  There are medications to relieve the symptoms.
Herpes simplex virus type 1 is different from genital herpes, which is herpes simplex virus type 2.
When will we see a herpes cure?
Researchers from University of Utah and the University of Massachusetts say the gene behind the frequent cold sores is C21orf91. Everyone has the gene, but there are two variations of the C21orf91 that are associated with the greater frequency of the outbreaks.
This doesn’t mean that people who have one of these two gene variations will automatically get a slew of cold sores.
“Twenty-one percent of the trait is due to genetic factors,” said study author, Dr. John Kriesel who is also a research associate professor of infectious diseases at the University of Utah School of Medicine. This means that 79% is due to other factors such as the virus strain and environmental factors.
Kriesel and the co-authors reached their findings after analysing data from the gene sequences from 618 study participants - half of whom had cold sore outbreaks.
“The hope is if we can figure out what this protein is doing, we’ll find insight,” Kriesel said.  “There are other forms of herpes that are much more serious than cold sores.”
Post by: Madison Park - CNNhealth.com Writer/Producer

Bacterial Friend?

Bdellovibrio bacteria act as 'living antibiotic' against important human pathogen

Scientists have found that a predatory bacterium significantly reduces the number of salmonella bacteria in the guts of live chickens, suggesting that the bacterium has potential to be used as a "living antibiotic."

Researchers at the University of Nottingham found that Bdellovibrio reduced the numbers of Salmonella by 90 percent and the birds remained healthy, grew well, and were generally in good condition.

Salmonella likes to grow in the guts of poultry and other animals and can cause food poisoning in humans.

Dr Laura Hobley said "Bdellovibrio has the potential to be used as a living antibiotic against some major human and animal pathogens, such as E. coli and other so-called Gram-negative bacteria."

She continued "We think that Bdellovibrio could be particularly useful as a topical treatment for wounds or foot rots but we wanted to know what might happen if it is ingested - either deliberately as a treatment, or by accident."

Previous studies have shown that Bdellovibrio is very effective at invading and killing other bacterial cells in a test tube.

And now it looks likely to provide an alternative to antibiotic medicines at a time when bacterial resistance is a significant problem to human and animal health.

Reference:R. J. Atterbury, L. Hobley, R. Till, C. Lambert, M. J. Capeness, T. R. Lerner, A. K. Fenton, P. Barrow, R. E. Sockett. Studying the effects of orally administered Bdellovibrio on the wellbeing and Salmonella colonization of young chicks.. Applied and Environmental Microbiology, 2011; DOI: 10.1128/AEM.00426-11


Professor Douglas Kell, Chief Executive, BBSRC said "Once we have understood the fundamental nature of an extraordinary organism such as Bdellovibrio, it makes sense that we should look at potential uses for it. The impact of bacterial infections on human and animal health is significant and since antibiotic resistance is a major issue, alternatives from nature may become increasingly important."

http://media.eurekalert.org/release_graphics/Bdellovibrio1_27_04_highres.jpg